Your browser doesn't support javascript.
loading
Show: 20 | 50 | 100
Results 1 - 20 de 55
Filter
1.
Acta cir. bras ; 33(12): 1043-1051, Dec. 2018. graf
Article in English | LILACS | ID: biblio-973484

ABSTRACT

Abstract Purpose: To analyze the effect of methylene blue (MB) therapy during the liver ischemia-reperfusion injury (I/R) process. Methods: Thirty-five male Wistar rats were used, (70%) submitted to partial ischemia (IR) or not (NIR) (30%) were obtained from the same animal. These animals were divided into six groups: 1) Sham (SH), 2) Sham with MB (SH-MB); 3) I/R, submitted to 60 minutes of partial ischemia and 15 minutes of reperfusion; 4) NI/R, without I/R obtained from the same animal of group I/R; 5) I/R-MB submitted to I/R and MB and 6) NI/R-MB, without I/R. Mitochondrial function was evaluated. Osmotic swelling of mitochondria as well as the determination of malondialdehyde (MDA) was evaluated. Serum (ALT/AST) dosages were also performed. MB was used at the concentration of 15mg/kg, 15 minutes before hepatic reperfusion. Statistical analysis was done by the Mann Whitney test at 5%. Results: State 3 shows inhibition in all ischemic groups. State 4 was increased in all groups, except the I/R-MB and NI/R-MB groups. RCR showed a decrease in all I/R and NI/R groups. Mitochondrial osmotic swelling showed an increase in all I/R NI/R groups in the presence or absence of MB. About MDA, there was a decrease in SH values in the presence of MB and this decrease was maintained in the I/R group. AST levels were increased in all ischemic with or without MB. Conclusions: The methylene blue was not able to restore the mitochondrial parameters studied. Also, it was able to decrease lipid peroxidation, preventing the formation of reactive oxygen species.


Subject(s)
Humans , Animals , Male , Reperfusion Injury/prevention & control , Enzyme Inhibitors/therapeutic use , Liver/blood supply , Methylene Blue/therapeutic use , Oxygen Consumption , Aspartate Aminotransferases/blood , Reference Values , Time Factors , Mitochondria, Liver/drug effects , Mitochondria, Liver/metabolism , Lipid Peroxidation/drug effects , Reperfusion Injury/metabolism , Reproducibility of Results , Reactive Oxygen Species/analysis , Reactive Oxygen Species/metabolism , Rats, Wistar , Cell Respiration , Alanine Transaminase/blood , Enzyme Inhibitors/pharmacology , Mitochondrial Membranes/drug effects , Mitochondrial Membranes/metabolism , Liver/metabolism , Malondialdehyde/analysis , Methylene Blue/pharmacology , Mitochondrial Swelling/drug effects
2.
Acta cir. bras ; 30(11): 749-755, Nov. 2015. tab, graf
Article in English | LILACS | ID: lil-767602

ABSTRACT

PURPOSE: To evaluate the underlying mechanisms by which sevoflurane protects the liver against ischemia/reperfusion injury evaluate the mechanism by which sevoflurane exerts this protective effect. METHODS: Twenty-six rats were subjected to partial ischemia/reperfusion injury for 1h: one group received no treatment, one group received sevoflurane, and sham group of animals received laparotomy only. Four hours after reperfusion, levels of alanine and aspartate aminotransferases, tumor necrosis factor-a, and interleukins 6 and 10 were measured. Analyses of mitochondrial oxidation and phosphorylation, malondialdehyde content, histology, and pulmonary vascular permeability were performed. RESULTS: Serum levels of alanine and aspartate aminotransferases were significantly lower in the sevoflurane group compared to untreated controls (p<0.05). The sevoflurane group also showed preservation of liver mitochondrial function compared to untreated controls (p<0.05). Sevoflurane administration did not alter increases in serum levels of tumor necrosis factor-a, and interleukins 6 and 10. Sevoflurane treatment significantly reduced the coagulative necrosis induced by ischemia/reperfusion (p<0.05). Pulmonary vascular permeability was preserved in the sevoflurane group compared to untreated controls. CONCLUSION: Sevoflurane administration protects the liver against ischemia/reperfusion injury, via preservation of mitochondrial function, and also preserves lung vascular permeability.


Subject(s)
Animals , Male , Anesthetics, Inhalation/pharmacology , Ischemia/prevention & control , Liver/blood supply , Methyl Ethers/pharmacology , Mitochondria, Liver/drug effects , Reperfusion Injury/prevention & control , Alanine Transaminase/blood , Aspartate Aminotransferases/blood , Capillary Permeability/drug effects , Cytokines/blood , Ischemia/pathology , Lipid Peroxidation , Liver/pathology , Mitochondria, Liver/physiology , Necrosis , Phosphorylation , Rats, Wistar , Reproducibility of Results , Reperfusion Injury/pathology , Time Factors
3.
Biol. Res ; 48: 1-6, 2015. graf
Article in English | LILACS | ID: biblio-950781

ABSTRACT

BACKGROUND: Karwinskia humboldtiana (Kh) is a poisonous plant of the rhamnacea family. To elucidate some of the subcellular effects of Kh toxicity, membrane fluidity and ATPase activities as hydrolytic and as proton-pumping activity were assessed in rat liver submitochondrial particles. Rats were randomly assigned into control non-treated group and groups that received 1,1.5 and 2 g/Kg body weight of dry powder of Kh fruit, respectively. Rats were euthanized at day 1 and 7 after treatment. RESULTS: Rats under Kh treatment at all dose levels tested, does not developed any neurologic symptoms. However, we detected alterations in membrane fluidity and ATPase activity. Lower dose of Kh on day 1 after treatment induced higher mitochondrial membrane fluidity than control group. This change was strongly correlated with increased ATPase activity and pH gradient driven by ATP hydrolysis. On the other hand, membrane fluidity was hardly affected on day 7 after treatment with Kh. Surprisingly, the pH gradient driven by ATPase activity was significantly higher than controls despite an diminution of the hydrolytic activity of ATPase. CONCLUSIONS: The changes in ATPase activity and pH gradient driven by ATPase activity suggest an adaptive condition whereby the fluidity of the membrane is altered.


Subject(s)
Animals , Male , Rats , Mitochondria, Liver/drug effects , Adenosine Triphosphatases/metabolism , Karwinskia/toxicity , Membrane Fluidity/drug effects , Subcellular Fractions/drug effects , Submitochondrial Particles/drug effects , Mitochondria, Liver/enzymology , Random Allocation , Rats, Sprague-Dawley , Proton-Motive Force/drug effects , Fruit/toxicity
4.
Rev. bras. parasitol. vet ; 23(4): 428-434, Oct-Dec/2014. tab, graf
Article in English | LILACS | ID: lil-731249

ABSTRACT

Three hemoplasma species are recognized in domestic cats: Mycoplasma haemofelis, ‘Candidatus Mycoplasma haemominutum’ and ‘Candidatus Mycoplasma turicensis’. We report the prevalence and hematological abnormalities of hemoplasma infection in 369 domestic cats from three different populations (blood donors, hospitalized cats and shelter cats) from Southern Brazil. Complete blood counts were performed at the time of blood collection, and DNA was extracted and tested by conventional PCR for each hemoplasma species. A total of 79 samples (21.40%) were positive for at least one species. The most prevalent hemoplasma was ‘Candidatus Mycoplasma haemominutum’, with 50/369 (13.55%) positive cats, followed by ‘Candidatus Mycoplasma turicensis’, 10/369 (2.71%), and Mycoplasma haemofelis, 8/369 (2.16%). Mycoplasma haemofelis and ‘Candidatus Mycoplasma haemominutum’ coinfection was observed in 4/369 (1.08%), whereas ‘Candidatus Mycoplasma haemominutum’ and ‘Candidatus Mycoplasma turicensis’ in 5/369 (1.35%). Three cats (0.81%) were infected with all three hemoplasmas. There was no association between infection and the different populations. Anemia was associated with Mycoplasma haemofelis and ‘Candidatus Mycoplasma haemominutum’, but not with ‘Candidatus Mycoplasma turicensis’. Male cats and cats with outdoor access were more likely to be infected. Although ‘Candidatus Mycoplasma haemominutum’ is believed to cause minimal or no hematological alterations, the infected cats studied herein were more likely to be anemic.


Três espécies de hemoplasmas são reconhecidas em gatos domésticos: Mycoplasma haemofelis, ‘Candidatus Mycoplasma haemominutum’ e ‘Candidatus Mycoplasma turicensis’. A prevalência e alterações hematológicas associadas à infecção por hemoplasmas foi estudada, em 369 gatos domésticos de três populações distintas (doadores de sangue, hospitais e gatos de abrigo) do Sul do Brasil. Foram realizados hemogramas completos no momento da coleta de sangue e as amostras tiveram seu DNA extraído e testado por PCR convencional para cada espécie de hemoplasmas. Setenta e nove amostras (21,40%) foram positivas para pelo menos uma espécie. O mais prevalente foi ‘Candidatus Mycoplasma haemominutum’ com 50/369 (13,55%) gatos positivos, seguidos por ‘Candidatus Mycoplasma turicensis’ com 10/369 (2,71%) e Mycoplasma haemofelis com 8/369 (2,16%). Coinfecção por Mycoplasma haemofelis e ‘Candidatus Mycoplasma haemominutum’ foi observada em 4/369 (1,08%), enquanto ‘Candidatus Mycoplasma haemominutum’ e ‘Candidatus Mycoplasma turicensis’ coinfectaram 5/369 (1,35%) gatos. Três (0,81%) gatos apresentaram infecção pelos três hemoplasmas. Não houve associação entre a infecção e as diferentes populações. Anemia foi associada com a infecção por Mycoplasma haemofelis e ‘Candidatus Mycoplasma haemominutum’, mas não com ‘Candidatus Mycoplasma turicensis’. Gatos machos e com acesso à rua apresentaram maior probabilidade de serem infectados. Embora se acredite que ‘Candidatus Mycoplasma haemominutum’ possa causar alterações hematológicas mínimas ou ausentes, gatos infectados encontrados neste estudo foram mais propensos à anemia.


Subject(s)
Animals , Male , Rats , Hepatocytes/drug effects , Mitochondria, Liver/drug effects , NAD(P)H Dehydrogenase (Quinone)/metabolism , Oxidative Stress/drug effects , Ubiquinone/pharmacology , Cells, Cultured , Cytoprotection , Cell Membrane/drug effects , Cell Survival/drug effects , Glutathione/metabolism , Hepatocytes/enzymology , Membrane Potentials/drug effects , Mitochondria, Liver/enzymology , NAD , Oxidation-Reduction , Rats, Sprague-Dawley , Reactive Oxygen Species/metabolism , Rotenone/toxicity , Uncoupling Agents/toxicity , /pharmacology
5.
Salud pública Méx ; 56(4): 402-404, jul.-ago. 2014. tab
Article in Spanish | LILACS | ID: lil-733306

ABSTRACT

La fiebre chikungunya (CHIK) es una enfermedad viral transmitida al ser humano por el mismo vector del dengue, el mosquito Aedes. Además de fiebre y fuertes dolores articulares, produce otros síntomas como mialgias, cefalea, náuseas, cansancio y exantema. No tiene tratamiento específico; el manejo terapéutico de los pacientes se enfoca en el alivio de los síntomas. Históricamente se han reportado brotes de grandes proporciones; incluso desde 2010 se llegó a considerar como una potencial epidemia emergente. En 2013 se introdujo a las islas del Caribe y recientemente se ha reportado en el continente americano. En este trabajo se describe el primer caso confirmado de chikungunya en México, en el municipio de Tlajomulco de Zúñiga, Jalisco, en mayo de 2014, importado de la isla Antigua y Barbuda, en el Caribe, por una mujer de 39 años de edad.


Chikungunya fever (CHIK) is a viral disease transmitted to human beings by the same vector as dengue -the Aedes mosquito. Besides fever and severe pain in the joints, it produces other symptoms such as myalgias, headache, nausea, fatigue and exanthema. There is no specific treatment for it; the therapeutic management of patients focuses on symptom relief. Historically, outbreaks of large proportions have been reported; even since 2010 it was considered to be a potential emerging epidemic. In 2013 it was introduced into the islands of the Caribbean, and it has recently been reported in the American continent. This paper describes the first confirmed case of chikungunya in Mexico -in the municipality of Tlajomulco de Zúñiga, Jalisco, in May, 2014-, which was imported from the Caribbean island of Antigua and Barbuda by a 39 year-old woman.


Subject(s)
Animals , Cattle , Male , Rats , Antidotes/pharmacology , Hot Temperature , Imidazoles/toxicity , Meat , Mitochondria/metabolism , Mutagens/toxicity , Oxygen Consumption/drug effects , Ubiquinone/pharmacology , Antidotes/administration & dosage , Cooking , Diet , Electron Transport Complex II , Electron Transport Complex III/metabolism , Electron Transport Complex IV/metabolism , Electron Transport/drug effects , Food, Fortified , Mitochondria, Heart/drug effects , Mitochondria, Heart/metabolism , Mitochondria, Liver/drug effects , Mitochondria, Liver/metabolism , Mitochondria, Muscle/drug effects , Mitochondria, Muscle/metabolism , Multienzyme Complexes/metabolism , NAD(P)H Dehydrogenase (Quinone)/metabolism , Oxidoreductases/metabolism , Rats, Wistar , Succinate Dehydrogenase/metabolism , Ubiquinone/administration & dosage
6.
Biol. Res ; 47: 1-8, 2014. graf
Article in English | LILACS | ID: biblio-950770

ABSTRACT

BACKGROUND: Nitrosative and oxidative stress play a key role in obesity and diabetes-related mitochondrial dysfunction. The objective was to investigate the effect of curcumin treatment on state 3 and 4 oxygen consumption, nitric oxide (NO) synthesis, ATPase activity and lipid oxidation in mitochondria isolated from liver and kidneys of diabetic db/db mice. RESULTS: Hyperglycaemia increased oxygen consumption and decreased NO synthesis in liver mitochondria isolated from diabetic mice relative to the control mice. In kidney mitochondria, hyperglycaemia increased state 3 oxygen consumption and thiobarbituric acid-reactive substances (TBARS) levels in diabetic mice relative to control mice. Interestingly, treating db/db mice with curcumin improved or restored these parameters to normal levels; also curcumin increased liver mitochondrial ATPase activity in db/db mice relative to untreated db/db mice. CONCLUSIONS: These findings suggest that hyperglycaemia modifies oxygen consumption rate, NO synthesis and increases TBARS levels in mitochondria from the liver and kidneys of diabetic mice, whereas curcumin may have a protective role against these alterations.


Subject(s)
Animals , Male , Mice , Lipid Peroxidation/drug effects , Curcumin/pharmacology , Diabetes Mellitus, Type 2/diet therapy , Kidney/drug effects , Liver/drug effects , Mitochondria/drug effects , Oxygen Consumption/drug effects , Body Weight/drug effects , Mitochondria, Liver/drug effects , Mitochondria, Liver/enzymology , Adenosine Triphosphatases/drug effects , Oxidative Stress/drug effects , Cell Respiration/drug effects , Dietary Supplements , Diabetes Mellitus, Type 2/complications , Diabetes Mellitus, Type 2/physiopathology , Disease Models, Animal , Selective Breeding , Genotype , Hyperglycemia/diet therapy , Hyperglycemia/etiology , Mitochondria/enzymology , Nitric Oxide/analysis , Nitric Oxide/metabolism
7.
Indian J Exp Biol ; 2013 Aug; 51(8): 623-634
Article in English | IMSEAR | ID: sea-149365

ABSTRACT

Achatina fulica C-reactive protein (ACRP) reversed the toxic effects of lead nitrate both in vivo in mice and in vitro in rat hepatocytes restoring the basal level of cell viability, lipid peroxidation, reduced glutathione and superoxides. Cytotoxicity was also significantly ameliorated in rat hepatocytes by in vitro pre-treatments with individual subunits (60, 62, 90 and 110 kDa) of ACRP. Annexin V-Cy3/CFDA dual staining showed significant reduction in the number of apoptotic hepatocytes pre-treated with ACRP. ACRP induced restoration of mitochondrial membrane potential was remarkable. ACRP pre-treatment prevented Pb-induced apoptosis mediated by caspase activation. The antagonistic effect of ACRP may be due to scavenging of reactive oxygen species which maintained the homeostasis of cellular redox potential as well as reduced glutathione status. The results suggest that ACRP crosses the species barrier and it may be utilized as a viable exogenous agent of cytoprotection against heavy metal related toxicity.


Subject(s)
Animals , Apoptosis/drug effects , Blotting, Western , C-Reactive Protein/pharmacology , Cell Survival , Cytoprotection/drug effects , Glutathione/metabolism , Hazardous Substances/toxicity , Hepatocytes/drug effects , Hepatocytes/pathology , Lead/toxicity , Lipid Peroxidation/drug effects , Male , Membrane Potential, Mitochondrial/drug effects , Mice , Mitochondria, Liver/drug effects , Mitochondria, Liver/pathology , Mollusca , Nitrates/toxicity , Oxidative Stress/drug effects , Rats , Rats, Sprague-Dawley , Reactive Oxygen Species/metabolism
8.
Acta cir. bras ; 27(7): 477-481, jul. 2012. tab
Article in English | LILACS | ID: lil-640096

ABSTRACT

PURPOSE: To investigate the effect of lovastatin on renal ischemia followed by reperfusion. METHODS: Thirty one Wistar rats submitted to left renal ischemia for 60 minutes followed by contralateral nephrectomy were divided into two groups: A (n =17, control, no treatment), and B (n=14, lovastatin 15 mg/kg/day p.o. ten days before ischemia). The animals were sacrificed at the end of ischemia, after 24 hours and at seven days after reperfusion. Survival, serum urea and creatinine levels and renal mitochondrial function were evaluated. RESULTS: Mortality was 29.4% in group A and 0.7% in group B. Urea and creatinine levels were increased in both groups, but the values were significantly lower in group B. Mitochondrial function showed decoupling in 83.4% of group A, as opposed to 38.4/% of group B. CONCLUSIONS: The result shows a protective action of renal function by lovastatin administered before ischemia/reperfusion. Since most of the mitochondrial fraction presented membranes with the ability to maintain ATP production in group B, stabilization of the mitochondrial membrane should be considered as part of the protective action of lovastatin on renal function in ischemia/reperfusion.


OBJETIVO: Investigar a ação da lovastatina na isquemia renal seguida de reperfusão. MÉTODOS: Trinta e um ratos Wistar submetidos à isquemia renal esquerda durante 60 minutos, seguida da nefrectomia contralateral, foram distribuídos em dois grupos: A (n=17, controle, sem tratamento) e B (n=14, recebendo 15 mg/Kg/dia de lovastatina via oral), durante os dez dias que antecederam a isquemia. Os animais foram mortos ao final da isquemia, e com 24 horas e sete dias após a reperfusão. Foram avaliadas a sobrevida, os valores séricos de uréia e creatinina e a função mitocondrial renal. RESULTADOS: A mortalidade foi 29,4% no grupo A e 0,7% no grupo B. Os níveis de uréia e creatinina elevaram-se nos dois grupos, mas foram significativamente menores no grupo B. No grupo A a função mitocondrial renal ficou desacoplada em 83,4% dos ensaios, enquanto que no grupo B isto ocorreu em apenas 38,4% dos ensaios. CONCLUSÕES: Os resultados mostram que a administração de lovastatina antes do episódio de isquemia protege a função renal. No grupo B, como a maior parte da fração mitocondrial isolada apresentou função acoplada à produção de ATP, deve-se também considerar a estabilização da membrana mitocondrial como parte da ação protetora da lovastatina na função renal durante isquemia e reperfusão.


Subject(s)
Animals , Male , Rats , Hypolipidemic Agents/pharmacology , Kidney/drug effects , Lovastatin/pharmacology , Mitochondria, Liver/drug effects , Reperfusion Injury/drug therapy , Creatinine/blood , Kidney/blood supply , Kidney/physiopathology , Mitochondria, Liver/physiology , Nephrectomy , Rats, Wistar , Renal Circulation/drug effects , Renal Circulation/physiology , Reperfusion Injury/blood , Reperfusion Injury/physiopathology , Time Factors , Urea/blood
9.
Indian J Biochem Biophys ; 2011 Aug; 48(4): 275-282
Article in English | IMSEAR | ID: sea-135329

ABSTRACT

Baicalein (5, 6, 7-trihydroxy-2-phenyl-4H-1-benzopyran-4-one), a naturally occurring flavone present in some of the medicinal plants is known for its potential therapeutic effects, such as cardioprotective, anticancer and anti-inflammatory properties. However, detailed role and mechanisms behind its protective properties against different generators for oxidative stress have not been examined. In the present study, we investigated the possible protective ability of baicalein against the membrane damage caused by reactive oxygen species (ROS) and reactive nitrogen species (RNS) and the mechanisms involved using pulse radiolysis technique. Baicalein offered efficient protection even at a concentration of 10 M towards membrane damage caused by lipid peroxidation induced by the -radiation, peroxyl radicals, ascorbate-Fe2+ and peroxynitrite in rat liver mitochondria and heart homogenate. To elucidate its reaction mechanisms with biologically relevant radicals, transient absorption spectroscopy employing pulse radiolysis technique was used. Baicalein showed fairly high rate constants (3.7 × 109, 1.3 × 109 and 8.0 × 108 dm3 mol-1 s-1 for hydroxyl, azidyl and alkylchloroperoxyl radicals, respectively), suggesting that baicalein can act as an effective scavenger of these radicals. In each case, the phenoxyl radical of baicalein was generated. Thus, it was evident that the phenolic moiety of baicalein was responsible for the free radical scavenging process. Baicalein also reacts with linoleic acid peroxyl radical (LOO·), indicating its ability to act as a chain breaking antioxidant. Peroxynitrite-mediated radicals were shown to be reactive towards baicalein and the bimolecular rate constants were 2.5 × 107 and 3 × 108 dm3 mol-1 s-1 for ·NO2 and CO3·- radicals, respectively. In conclusion, our results revealed the potential of baicalein in protecting mitochondrial membrane against oxidative damage induced by the four different agents. We propose that the protective effect is mediated via scavenging of primary and secondary radicals generated during oxidative stress.


Subject(s)
Animals , Cell Membrane/drug effects , Female , Flavanones/chemistry , Flavanones/pharmacology , Free Radicals , Heart/drug effects , Mitochondria, Liver/drug effects , Rats , Rats, Wistar , Reactive Oxygen Species/metabolism
10.
Indian J Exp Biol ; 2008 Feb; 46(2): 112-9
Article in English | IMSEAR | ID: sea-62933

ABSTRACT

To assess the oxidative stress and mitochondrial dysfunction associated with disease, toxic process and aging, in vivo and in vitro preventive effect of propolis extract against mitochondrial oxidative stress induced by two anticancer drugs (doxorubicin and vinblastin) have been investigated in female wistar rat using liver and heart mitochondria. The results show that doxorubicin and vinblastin altered mitochondrial functions as observed by a decrease in respiratory control value, an activation of swelling and overproduction of superoxide anion. Myocardial tissue from doxorubicin treated rats showed a marked increase in malondialdehyde production, a depletion of reduced glutathione contents and an inhibition of catalase and superoxide dismutase activities. Similar results were also observed in liver tissue. Pretreatment of rats with propolis extract (100 mg/kg/day po) (10(-4) M ip) administered 4 days prior to doxorubicin (20 mg/kg) and/or vinblastin (2 mg/kg) injection, substantially reduced the peroxidative damage in myocardium and hepatic tissues and markedly restored the tissues catalase and SOD activities. The results strongly suggest that propolis extract protects heart and liver tissues from oxidative stress by protecting the mitochondria.


Subject(s)
Animals , Antineoplastic Agents/toxicity , Antioxidants/chemistry , Catalase/metabolism , Complex Mixtures/pharmacology , Disease Models, Animal , Doxorubicin/toxicity , Drug-Related Side Effects and Adverse Reactions/drug therapy , Female , Lipid Peroxidation/drug effects , Mitochondria, Heart/drug effects , Mitochondria, Liver/drug effects , Oxidative Stress/drug effects , Propolis/chemistry , Quercetin/analysis , Rats , Rats, Wistar , Superoxide Dismutase/metabolism , Vinblastine/toxicity
11.
An. acad. bras. ciênc ; 78(3): 505-514, Sept. 2006. graf
Article in English | LILACS | ID: lil-433717

ABSTRACT

Desequilíbrio/acúmulo de ferro tem sido implicado em injúria oxidativa associada a diversas doenças degenerativas tais como, hemocromatose hereditária, b-talassemia e ataxia de Friedreich. As mitocôndrias são particularmente sensíveis a estresse oxidativo induzido por ferro - um carregamento alto de ferro em mitocôndrias isoladas pode causar uma extensiva peroxidação lipídica e a permeabilização de membrana. Nesse estudo, nós detectamos e caracterizamos danos do DNA mitocondrial em mitocôndrias isoladas de fígado de rato, expostas ao complexo Fe2+-citrato, um dos complexos de baixo peso molecular. A intensa fragmentação do DNA foi induzida após a incubação das mitocôndrias com o complexo de ferro. A detecção de finais 3' de fosfoglicolato nas quebras de fitas de DNA mitocondrial pelo ensaio 32P-postlabeling sugere um envolvimento de radicais hidroxila na fragmentação do DNA induzido por complexo Fe2+-citrato. Os níveis elevados de 8-oxo-7,8-diidro-2'-desoxiguanosina também sugerem que o estresse oxidativo induzido por Fe2+-citrato causa danos no DNA mitocondrial. Em conclusão, nossos resultados mostram que a peroxidação lipídica mediada por ferro esteve associada com severos danos do DNA mitocondrial derivados de ataque direto das espécies reativas de oxigênio.


Subject(s)
Animals , Male , Rats , DNA Damage , DNA, Mitochondrial/drug effects , Ferrous Compounds/pharmacology , Lipid Peroxidation/drug effects , Mitochondria, Liver/drug effects , DNA, Mitochondrial/metabolism , Mitochondria, Liver/metabolism , Mitochondrial Membranes/drug effects , Mitochondrial Membranes/metabolism , Mitochondrial Swelling/drug effects , Rats, Wistar
12.
Indian J Biochem Biophys ; 2005 Dec; 42(6): 345-9
Article in English | IMSEAR | ID: sea-27399

ABSTRACT

The activities of malate-aspartate shuttle enzymes viz., cytosolic and mitochondrial aspartate aminotransferase (c- and m-AsAT) and malate dehydrogenase (c- and m-MDH) were measured in liver and kidney of ad libitum (AL) and dietary-restricted (DR) mice and also on triiodothyronine (T3) treatment. The results show that the activity (U/mg protein) of c-AsAT is increased significantly in liver and the activities of c-MDH and m-AsAT are increased significantly in kidney during DR. On T3 treatment, the activities of both the isoenzymes (c- and m-) of MDH and AsAT are increased significantly in the liver of AL- and DR-fed mice. In the kidney, m-MDH showed no effect by T3 treatment, however, c-MDH increased significantly in both AL- and DR-fed mice. In contrast, m-AsAT is increased significantly in the kidney in AL-fed mice, but was not affected in DR-fed animals. In vitro reconstitution of malate-aspartate shuttle showed a higher activity in the liver and kidney of DR-fed mice, as compared to AL-fed ones and also in the T3-treated mice, compared to untreated ones. These findings suggest that malate-aspartate shuttle enzymes are differentially regulated during DR in mice, in order to adapt to the metabolic need of liver and kidney. T3 potentially regulates the shuttle enzymes, albeit to a varying degree in the liver and kidney of AL- and DR-fed mice.


Subject(s)
Animals , Aspartate Aminotransferases/metabolism , Aspartic Acid/metabolism , Caloric Restriction , Cytosol/drug effects , Diet , Isoenzymes/metabolism , Kidney/drug effects , Liver/drug effects , Malate Dehydrogenase/metabolism , Malates/metabolism , Male , Mice , Mice, Inbred BALB C , Mitochondria, Liver/drug effects , Triiodothyronine/pharmacology
13.
Acta cir. bras ; 20(supl.1): 72-77, 2005.
Article in English | LILACS | ID: lil-414639

ABSTRACT

OBJETIVO: Testar a hipótese do catecol inibir a respiração basal associada ao FADH2 em frações mitocondriais hepáticas de rato. Além disso, estudou-se também a capacidade do catecol de induzir peroxidação de biomoléculas nas frações nucleares. MÉTODOS: Os homogeneizados de fígado de ratos foram incubados com catecol a 1 mM em pH fisiológico. Depois disso, as frações mitocondriais foram isoladas por centrifugação diferencial. O consumo basal de oxigênio foi medido com um eletrodo do tipo Clark após injeção de succinato a 10 mM. Frações nucleares foram incubadas com catecol por 17 horas à temperatura ambiente e a peroxidação de biomoléculas foi investigada pela reação com o ácido tiobarbitúrico e mensurada espectrofotometricamente. RESULTADOS: O catecol induziu uma inibição parcial da respiração basal mitocondrial associada ao FADH2 de forma dependente do tempo, contudo essa substância não induziu peroxidação direta das biomoléculas presentes nas frações nucleares hepáticas. CONCLUSÃO: O catecol produz inibição da respiração basal associada ao FADH2 em mitocôndrias isoladas de fígado, o que pode levar à toxicidade, produção de espécies reativas e morte celular.


Subject(s)
Animals , Rats , Catechols/toxicity , Flavin-Adenine Dinucleotide/analogs & derivatives , Lipid Peroxidation/drug effects , Mitochondria, Liver/drug effects , Oxidative Stress/drug effects , Oxygen Consumption/drug effects , Cell Nucleus/drug effects , Cell Respiration/drug effects , Enzyme Inhibitors/pharmacology , Flavin-Adenine Dinucleotide/antagonists & inhibitors , Mitochondria, Liver/metabolism , Rats, Wistar , Reactive Oxygen Species/metabolism , Time Factors
14.
Braz. dent. j ; 14(1): 32-36, June 2003. ilus, tab
Article in English | LILACS | ID: lil-340486

ABSTRACT

Copper/aluminum alloys are largely utilized in odontological restorations because they are less expensive than gold or platinum. However, tarnishing and important corrosion in intrabuccal prostheses made with copper/aluminum alloys after 28 days of use have been reported. Several kinds of food and beverage may attack and corrode these alloys. Copper is an essential component of several important enzymes directly involved in mitochondrial respiratory metabolism. Aluminum, in contrast, is very toxic and, when absorbed, plasma values as small as 1.65 to 21.55 µg/dl can cause severe lesions to the nervous system, kidneys, and bone marrow. Because mitochondria are extremely sensitive to minimal variation of cellular physiology, the direct relationship between the mitocondrial respiratory chain and cell lesions has been used as a sensitive parameter to evaluate cellular aggression by external agents. This work consisted in the polarographic study of mitochondrial respiratory metabolism of livers and kidneys of rabbits with femoral implants of titanium or copper/aluminum alloy screws. The experimental results obtained did not show physiological modifications of hepatic or renal mitochondria isolated from animals of the three experimental groups, which indicate good biocompatibility of copper/aluminum alloys and suggest their odontological use


Subject(s)
Animals , Male , Rabbits , Alloys/chemistry , Aluminum/chemistry , Biocompatible Materials/chemistry , Copper/chemistry , Mitochondria/metabolism , Bone Screws , Corrosion , Dental Materials/chemistry , Femur/surgery , Kidney/drug effects , Kidney/metabolism , Mitochondria, Liver/drug effects , Mitochondria, Liver/metabolism , Mitochondria/drug effects , Oxygen Consumption/drug effects , Oxygen Consumption/physiology , Polarography , Statistics as Topic , Surface Properties , Subcellular Fractions/drug effects , Subcellular Fractions/metabolism , Titanium/chemistry
15.
Indian J Exp Biol ; 2003 Apr; 41(4): 336-40
Article in English | IMSEAR | ID: sea-57416

ABSTRACT

Mitochondrial proteins and phospholipids were estimated and SDH, Na(+)-K(+)-ATPase and Mg(2+)-ATPase activities were analysed in the gill, liver and heart tissues of PCB 1232 (sublethal doses) treated fish A. caelatus. Protein and phospholipids were found to be decreased significantly and SDH, Na(+)-K(+)-ATPase, Mg(2+)-ATPase and other enzyme systems displayed an inverse relationship with PCB dosage. Statistical analysis was carried out to indicate the relationship between sublethal doses of varying concentration and the activities of the enzyme systems involved in energy metabolism. The studies indicated impairment in mitochondrial functions.


Subject(s)
Animals , Ca(2+) Mg(2+)-ATPase/metabolism , Catfishes/metabolism , Energy Metabolism , Gills/drug effects , Heart/drug effects , Liver/drug effects , Mitochondria, Heart/drug effects , Mitochondria, Liver/drug effects , Mitochondrial Proteins/metabolism , Phospholipids/metabolism , Polychlorinated Biphenyls/toxicity , Sodium-Potassium-Exchanging ATPase/metabolism , Succinate Dehydrogenase/metabolism
16.
Biocell ; 26(2): 237-245, Aug. 2002.
Article in English | LILACS | ID: lil-335848

ABSTRACT

CG 10-248 (3,4-dihydro-2,2 dimethyl-9-chloro-2H-naphtho[1,2b]pyran-5,6-dione), a beta-lapachone analogue, modified the ultrastructure of rat liver mitochondria in vitro, in the absence of added oxidizable substrates. The condensed mitochondrial state was replaced by the orthodox or swollen state to a significant degree. The number of modified mitochondria depended on incubation time and quinone concentration, in the 25-100 microM range. Under the same experimental conditions, mitochondrial respiration was uncoupled as indicated by the increase in the rate of succinate oxidation by controlled mitochondria in metabolic state "4" (not in state "3"), and by the activation of latent F0F1-ATP synthase. Taking into account structural similarities, the results reported here may be valid for other o-naphthoquinones, such as beta-lapachone.


Subject(s)
Animals , Male , Rats , Mitochondria, Liver/drug effects , Naphthoquinones , Proton-Translocating ATPases/metabolism , Hydrolysis , Mitochondria , Mitochondria, Liver/ultrastructure , Oxygen/metabolism , Quinones , Rats, Wistar , Structure-Activity Relationship , Time Factors
17.
Indian J Physiol Pharmacol ; 2002 Jul; 46(3): 343-8
Article in English | IMSEAR | ID: sea-107898

ABSTRACT

The effect of various concentrations of ursodeoxycholic acid (UDCA), a potent hepatoprotective agent on hydrogen peroxide-induced mitochondrial swelling was evaluated in vitro to find out the mechanism of action of the drug. Aliquots of sheep liver mitochondria were pre-incubated with various concentrations of UDCA [0-600 micrograms] and swelling was induced by hydrogen peroxide [1 mM]. Swelling was assessed at various time intervals and lipid peroxide, reduced glutathione status were also evaluated simultaneously. UDCA minimized hydrogen peroxide-induced swelling in a dose-dependent manner. Time-dependent elevation in the level of lipid peroxides was noted in mitochondria treated with hydrogen peroxide and this elevation was minimized in UDCA pre-treatment. UDCA also maintains the reduced glutathione level in mitochondria. UDCA acts against the oxidative stress imposed in liver mitochondria. It reduces lipid peroxidation-induced abnormalities such as swelling and thiol group depletion and the anti lipid peroxidative efficacy of the drug may be related to its hydrophilic nature which might protect the hydrophobic regions of the mitochondrial membranes which are prone for free radical-mediated reactions.


Subject(s)
Animals , Antioxidants/pharmacology , Hydrogen Peroxide/pharmacology , Lipid Peroxidation , Mitochondria, Liver/drug effects , Mitochondrial Swelling/drug effects , Sheep , Time Factors , Ursodeoxycholic Acid/pharmacology
18.
Indian J Exp Biol ; 1999 Nov; 37(11): 1139-41
Article in English | IMSEAR | ID: sea-59349

ABSTRACT

Cytochrome c oxidase was purified from control and CCl4 treated rats and its kinetic properties were studied. The activity of the enzyme was inhibited by 51% in CCl4 (4 g per kg body weight for 24 hr) treated rats. Studies on the kinetic properties showed that the K(m) of the enzyme increased by 60% while Vmax decreased by 44% in CCl4 treated rats compared to controls. The content of cytochrome aa3 was decreased by 34% while cytochrome b and c were not affected by CCl4 treatment. Phosphatidylcholine, phosphatidylethanolamine and cardiolipin were decreased significantly by 40%, 49% and 60% respectively in CCl4 treated rats. A decrease in the cytochrome aa3 content and a change in the lipid environment of the membrane are probably responsible for a decreased rate of electron transfer from cytochrome c to oxygen.


Subject(s)
Animals , Carbon Tetrachloride/toxicity , Electron Transport Complex IV/metabolism , Kinetics , Male , Mitochondria, Liver/drug effects , Rats , Rats, Wistar
19.
Indian J Exp Biol ; 1999 Sep; 37(9): 876-80
Article in English | IMSEAR | ID: sea-61868

ABSTRACT

A single dose of aflatoxin B1 (7 mg/kg body wt) to male rats significantly stimulated the turnover of mitochondrial phosphoinositides 1-7 hr following its administration. The elevation of phosphatidylinositol 3,4,5-trisphosphate was most pronounced whose level continued to be moderately high even at 17 hr period. The level of diacylglycerol showed a marked increase from 4 hr till 7 hr after carcinogen treatment, whereas that of inositol 1,4,5-trisphosphate recorded an increase with a maximum at 7 hr followed by a gradual decrease to near normal level at 24 hr period. The activation of phosphatidylinositol cycle together with an activation of PI 3-kinase, whose product PIP3 is known to be involved in apoptosis might contribute to the early step in the manifestation of toxicity and/or carcinogenicity.


Subject(s)
Aflatoxin B1/administration & dosage , Animals , Male , Mitochondria, Liver/drug effects , Phosphatidylinositols/metabolism , Rats , Rats, Wistar , Signal Transduction
20.
Indian J Exp Biol ; 1997 Nov; 35(11): 1187-90
Article in English | IMSEAR | ID: sea-59481

ABSTRACT

Isolated rat liver mitochondria were incubated with various concentrations of aflatoxin B (AFB) for different periods of time. Respiration rates were then measured with two substrates (succinate and glutamate). State 3 respiration rate (with added ADP) declined with increase in preincubation concentrations of AFB1 (0.15-0.50 mM). On the other hand, state 4 respiration rate (after depletion of added ADP) was found to increase with increased pretreatment concentration of AFB. As a consequence, respiratory control index was reduced attaining minimum value with 0.25 mM AFB and preincubation time of 10 min. The induced anomaly in mitochondrial respiratory functions appear to be due to membrane damage caused by interaction of reactive AFB1 metabolite generated by mitochondrial cytochrome P-450 enzymes with mitochondrial components.


Subject(s)
Aflatoxin B1/pharmacology , Animals , Carcinogens/pharmacology , Cells, Cultured , Male , Mitochondria, Liver/drug effects , Oxygen Consumption/drug effects , Rats , Rats, Wistar
SELECTION OF CITATIONS
SEARCH DETAIL