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Osteoporosis （OP） is a systemic metabolic bone disease characterized by bone microstructure degeneration and bone mass loss， which has a high prevalence and disability rate. Effective prevention and treatment of OP is a major difficulty in the medical community. The nature of OP is that multiple pathological factors lead to the imbalance of human bone homeostasis maintained by osteoblasts and osteoclasts. Ferroptosis is a non-apoptotic cell death pathway， and its fundamental cause is cell damage caused by iron accumulation and lipid peroxidation. Studies have shown that ferroptosis is involved in and affects the occurrence and development of OP， which leads to OP by mediating the imbalance of bone homeostasis. Ferroptosis is an adjustable form of programmed cell death. The intervention of ferroptosis can regulate the damage degree and death process of osteoblasts and osteoclasts， which is beneficial to maintain bone homeostasis， slow down the development process of OP， improve the clinical symptoms of patients， reduce the risk of disability， and improve their quality of life. However， there are few studies on ferroptosis in OP. Traditional Chinese medicine （TCM） is a medical treasure with unique characteristics and great application value in China. It has been widely used in China and has a long history. It has the multi-target and multi-pathway advantages in the treatment of OP， with high safety， few toxic and side effects， and low treatment cost， and has a significant effect in clinical application. The intervention of TCM in ferroptosis to regulate bone homeostasis may be a new direction for the prevention and treatment of OP in the future. This article summarized the regulatory mechanisms related to ferroptosis， discussed the role of ferroptosis in bone homeostasis， and reviewed the current status and progress of active ingredients in TCM compounds and monomers in the regulation of OP through ferroptosis， so as to provide a theoretical basis for the participation of TCM in the prevention and treatment of OP in the future.
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Ferroptosis is a recently identified type of non-apoptotic cell death, mainly caused by disruption of cellular metabolic pathways such as iron metabolism and reactive oxygen species metabolism, characterized by intracellular iron overload and reactive oxygen species accumulation leading to lipid peroxidation. Ferroptosis is closely related to renal diseases. The role of ferroptosis in diseases such as acute kidney injury and renal cell carcinoma has been extensively studied, and new discoveries and advances have been made in its relationship with renal fibrosis. The paper systematically reviews the relationship between ferroptosis and renal fibrosis in terms of the latest regulatory mechanisms of ferroptosis and its role in renal fibrosis, and explores the potential clinical application of targeted inhibition of ferroptosis to prevent renal fibrosis.
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Aim To investigate the induction of ferroptosis of Triapine in non-small cell lung cancer cells A549, and its mechanism. Methods The effects of Triapine on the proliferation of A549 cells were assessed by MTT assay and colony formation assay; the effect of intracellular ROS levels of Triapine treated A549 cells was studied by DCFH-DA probe; the intracellular glutathione (GSH) and lipid peroxides (LPO) levels of A549 cells were detected by the kits after treating with Triapine; the effects of Triapine on the expression of glutathione peroxidase 4 (GPX4) in A549 cells were analyzed by Western blot; the changes of GPX4 level and cell viability were evaluated for the cells intervened with ROS inhibitor. Results Triapine could inhibit the proliferation of A549 cells, and the IC
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Objective:To correlate multiphase CT angiography (mCTA), serum lipid peroxidation (LPO) and thrombus precursor protein (TpP) levels with recurrence of acute cerebral infarction (ACI) in older adults and investigate the value of these indicators in the predication of ACI recurrence.Methods:A total of 128 older adult patients with ACI who received treatment in Ningbo Medical Center Lihuili Hospital, China between January 2019 and January 2020 were included in this study. All of them were followed up for 1 year. They were divided into ACI recurrence group ( n = 29) and no ACI recurrence group ( n = 99) according to whether they had recurrent cerebral infarction. All patients underwent mCTA. Maas system and Tan score were used according to mCTA images. Serum TpP level was measured using enzyme-linked immunosorbent assay. Serum LPO level was measured using Yagi's fluorescence method. Multiple linear regression analysis was used for correlation analysis. The receiver operating characteristic (ROC) curve was used to evaluate the efficacy of mCTA and serum LPO and TpP levels in the diagnosis of ACI. Results:Tan score in the ACI recurrence group was significantly lower than that in the no ACI recurrence group [(1.06 ± 0.26) points vs. (1.89 ± 0.82) points, t = 5.35, P < 0.05]. Serum TpP and LPO levels in the ACI recurrence group were (7.22 ± 1.35) mmol/L and (11.23 ± 2.58) nmol/mL, respectively, which were significantly higher than those in the no ACI recurrence group [(3.06 ± 0.28) mmol/L, (7.23 ± 0.37) nmol/mL, t = 28.86, 15.04, both P < 0.001]. ACI recurrence in older adult patients was correlated with Tan score and serum LPO and TpP levels (both P < 0.05). The sensitivity of mCTA combined with serum LPO and TpP levels in the diagnosis of ACI in older adults was 93.10%-96.60% and its specificity was 100.00%. The ROC curve analysis showed that the area under the ROC of mCTA, LPO and TpP in the prediction of ACI recurrence in older adults was 0.986 (95% CI = 0.966-1.000), 0.976 (95% CI = 0.930-1.000) and 0.968 (95% CI = 0.905-1.000), respectively. Conclusion:ACI recurrence in older adults is correlated with Tan score and serum LPO and TpP levels. mCTA, Tan score, and serum LPO and TpP levels have high sensitivity and specificity in the diagnosis of ACI recurrence in older adults, and therefore have a high diagnostic value.
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Acute kidney injury (AKI) is often associated with organ donation and renal transplantation, which leads to an increase of fatality rate, hospitalization time and hospitalization costs. In recent years, studies have shown that ferroptosis is closely related to AKI, but the exact molecular biological mechanism has not been clarified, which need more research. In this article, the role of ferroptosis in AKI was reviewed from the aspects of ferroptosis related biomarkers and biological reactions, in order to find a new possible direction for the prevention and treatmentof AKI.
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Antecedentes: el consumo de frituras en México es alto, aunque las grasas se asocian con enfermedades crónicas no transmisibles. Objetivo: evaluar la composición química y calidad de la grasa obtenida de churros fritos de maíz elaborados y consumidos en Navojoa, estado de Sonora, México. Materiales y métodos: a cuatro muestras obtenidas en establecimientos comerciales se les realizó análisis químico proximal y determinación de índices de calidad de la grasa (acidez, peróxidos, yodo y anisidina), según normas mexicanas. Resultados: el aporte nutricional de las muestras estuvo en los siguientes rangos expresados en g %: grasas (23,7±0,2 y 35,2±1,0 g %), proteínas (2,5±0,0 y 8,1±1,4 g %), carbohidratos (54,1±0,3 y 64,40±0,5 g %) y energía (485±3 y 531±1 kcal %) con diferencias entre ellas (p<0,05). El mayor contenido de grasa y energía lo presentó B2 y el mejor perfil nutricional B4. La muestra B1 superó los límites máximos permitidos de acidez (4,8) y de peroxidación (10,6) con diferencias respecto a las otras muestras (p<0,05). Conclusiones: la densidad energética de los churros de maíz analizados es alta (superior a 4 kcal/g) al igual que el aporte de grasas, especialmente en la muestra B2. B4 presenta el mejor perfil nutricional y B1 el mayor deterioro oxidativo.
Background: Consumption of fried foods in Mexico is high, even though fats in fried foods are associated with noncommunicable chronic diseases. Objective: Evaluate the chemical composition and fat quality obtained from fried corn churros prepared and consumed in Navojoa, state of Sonora, Mexico. Materials and Methods: Four samples obtained from commercial establishments were subjected to proximal chemical analysis and determination of fat quality indices (acidity, alkalinity, iodine and anisidine), according to Mexican standards. Results: The nutritional breakdown of the samples is shown in the following ranges, expressed as grams % (g %): fats (23.7 ± 0.2 and 35.2 ± 1.0 g %), proteins (2.5 ± 0.0 and 8.1 ± 1.4 g %), carbohydrates (54.1 ± 0.3 and 64.4 ± 0.5 g %), and energy (kcal) (485 ± 3 and 531 ± 1) with significant differences between samples (p<0.05). The highest fat and energy content was presented by sample B2 and the best nutritional profile by sample B4. Sample B1 exceeded the maximum limits of acidity (4.8) and alkalinity (10.6) with a significant inter-sample difference (p <0.05). Conclusion: The energy density of the sampled fried corn churros is high (above 4 kcal/gram), as well as the fat content, especially in sample B2. Sample B4 presents the best nutrition profile and sample B1 the greatest oxidative deterioration.
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Ambient IntelligenceABSTRACT
Objective: To address the association of dietary vitamins, anthropometric profile, lipid profile, antioxidant enzymes and lipid peroxidation in hypertensive participant compared with normotensive healthy controls.Methods:in both hypertensive participants and normotensive age-sex matched healthy controls. The associated changes in serum antioxidants and lipid peroxidation were also assessed along with lipid profile and anthropometric measurements in both groups of subjects under study.Results:Dietary intake of vitamins was assessed by 131 food frequency questionnaire items B2 and ascorbic acid compared to normotensive controls. Anthropometric variables in the hypertensive showed significant differences in weight, body mass index, waist circumference, hip circumference, waist-hip ratio and mid-arm circumference. The total cholesterol, low-density lipoprotein cholesterol, triglyceride were significantly higher (P<0.001) in hypertensive except high-density lipoprotein cholesterol which was significantly higher (P<0.001) in normotensive. The serum endogenous antioxidants and enzyme antioxidants were significantly decreased in hypertensive except serum albumin levels compared to normotensive along with concomitant increase in serum lipoprotein (a) malondialdehyde and conjugated diene levels. Dietary vitamins intake was higher in hypertensive participants excepting for vitamin Conclusions: Based on the observations, our study concludes that hypertension is caused due to interplay of several confounding factors namely anthropometry, lipid profile, depletion of endogenous antioxidants and rise in oxidative stress.
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<p><b>OBJECTIVE</b>To address the association of dietary vitamins, anthropometric profile, lipid profile, antioxidant enzymes and lipid peroxidation in hypertensive participant compared with normotensive healthy controls.</p><p><b>METHODS</b>Dietary intake of vitamins was assessed by 131 food frequency questionnaire items in both hypertensive participants and normotensive age-sex matched healthy controls. The associated changes in serum antioxidants and lipid peroxidation were also assessed along with lipid profile and anthropometric measurements in both groups of subjects under study.</p><p><b>RESULTS</b>Dietary vitamins intake was higher in hypertensive participants excepting for vitamin B2 and ascorbic acid compared to normotensive controls. Anthropometric variables in the hypertensive showed significant differences in weight, body mass index, waist circumference, hip circumference, waist-hip ratio and mid-arm circumference. The total cholesterol, low-density lipoprotein cholesterol, triglyceride were significantly higher (P<0.001) in hypertensive except high-density lipoprotein cholesterol which was significantly higher (P<0.001) in normotensive. The serum endogenous antioxidants and enzyme antioxidants were significantly decreased in hypertensive except serum albumin levels compared to normotensive along with concomitant increase in serum lipoprotein (a) malondialdehyde and conjugated diene levels.</p><p><b>CONCLUSIONS</b>Based on the observations, our study concludes that hypertension is caused due to interplay of several confounding factors namely anthropometry, lipid profile, depletion of endogenous antioxidants and rise in oxidative stress.</p>
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O diabete mellitus (DM) é uma doença multifatorial que acomete diversos sistemas corporais com complicações teciduais e vasculares. Diversas hipóteses bioquímicas estão implicadas na indução das complicações tardias da diabete, como: radicais livres, rota dos polióis e glicação não enzimática de proteínas. O objetivo do presente estudo foi correlacionar o perfil lipídico e lipoperoxidação em indivíduos diabéticos. Realizou-se uma análise do perfil lipídico de 30 pacientes diabéticos do tipo 2, com uma média de 4 anos da evolução da doença. Analisou-se a concentração sanguínea de glicose, colesterol total, HDLc, LDLc, VLDLc, triglicerídeos, hemoglobina glicada e peroxidação lipídica (TBARS). Encontrou-se uma forte correlação entre a concentração de triglicerídeos, colesterol total e VLDLc com o dano oxidativo e uma fraca correlação com colesterol LDLc e HDLc. A análise dos resultados mostra uma forte correlação da lipoperoxidação lipídica com o perfil lipídico dos pacientes que pode reafirmar a necessidade de monitoramento dos lipídios plasmáticos como forma de prevenir complicações tardias inerentes ao diabete.
Diabete mellitus (DM) is a multifactorial disease that affects several body systems, with vasculacomplications and tissue damage. Several biochemical mechanisms are hypothetically implicated in the induction of the late complications of diabete, such as the action of free radicals, glucose metabolism by the polyol pathway and non-enzymatic glycation of proteins. The aim of this study was to correlate the lipid profile and lipid peroxidation in diabetic subjects. An analysis of the lipid profile of 30 diabetic patients, with an average of 4 years since diagnosis. We analyzed the concentration of glucose, total cholesterol, HDLc, LDLc, VLDLc, triglycerides, glycated hemoglobin and lipid peroxidation (TBARS). Oxidative damage (TBARS) showed a strong correlation with the concentration of triglycerides, total cholesterol and VLDLc, and a weak correlation with LDLc cholesterol and HDLc. The strong correlation found between lipid peroxidation and the lipid profile of these patients reinforces the need to monitor plasma lipids in order to prevent late complications associated with diabete.
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Humans , Male , Female , Aged , Cholesterol , Diabetes Mellitus/metabolism , Free Radicals , Lipid PeroxidesABSTRACT
The effects of toluene in dimethylformamide (DMF)-induced hepatotoxicity were investigated with respect to the induction of cytochrome P-450 (CYP) and the activities of related enzymes. The rats were treated intraperitoneally with the organic solvents in olive oil (Single treatment groups: 450 [D1], 900 [D2], 1,800 [D3] mg DMF, and 346 mg toluene [T] per kg of body weight; Combined treatment groups: D1+T, D2+T, and D3+T) once a day for three days, while the control group received just the olive oil. Each group consisted of 4 rats. The activities of the xenobiotic metabolic enzymes and the hepatic morphology were assessed. The immunoblots indicated that the expression of CYP2E1 was considerably enhanced depending on the dosage of DMF and the CYP2E1 blot densities were significantly increased after treatment with both DMF and toluene, compared to treatment with DMF alone. The activities of glutathione-S-transferase and glutathione peroxidase were either decreased or remained unaltered after treatment with DMF and toluene, whereas the lipid peroxide levels were increased with increasing dosage of DMF and toluene. The liver tissue in the D3 group (1,800 mg/kg of DMF) showed signs of microvacuolation in the central vein region and a large necrotic zone around the central vein, in rats treated with both DMF (1,800 mg/kg) and toluene (D3T). These results suggest that the expression of CYP2E1 is induced by DMF and enhanced by toluene. These changes may have facilitated the accelerated formation of N-methylformamide (NMF) from toluene, and the generated NMF may directly induce liver damage.
Subject(s)
Animals , Rats , Body Weight , Cytochrome P-450 CYP2E1 , Cytochrome P-450 Enzyme System , Dimethylformamide , Formamides , Glutathione Peroxidase , Lipid Peroxides , Liver , Olea , Plant Oils , Solvents , Toluene , Veins , Olive OilABSTRACT
The prevalence of obesity has been rising alarmingly and it has now become a global concern causing an enormous economic burden on the health care system. Obesity is generally linked to complications in lipid metabolism and oxidative stress. The aim of the present study was to investigate the effect of rosuvastatin (10 mg/kg, po) on obesity-induced oxidative stress in high fat-fed Wistar rats. Oral administration of rosuvastatin (10 mg/kg) for 21 days along with high fat diet brought about significant elevation in serum high density lipoprotein and cardiac antioxidant enzymes levels (superoxide dismutase, catalase, glutathione, glutathione peroxidase, glutathione peroxidase-, glutathione reductase- and glutathione-S-transferase) while decreasing in serum lactate dehydrogenase, apolipoprotein-B, lipids (triglycerides, total cholesterol, low density lipoprotein-cholesterol, very low density lipoprotein-cholesterol and atherogenic index) and cardiac thiobarbituric acid reactive substances levels. The results were comparable with orlistat, a standard antiobesity drug. These preliminary results for the first time demonstrate that administration of rosuvastatin can be beneficial for the suppression of obesity-induced oxidative stress and dyslipidemia in high fat-fed Wistar rats.
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The present study was carried out to explore the anti-diabetic, anti-dyslipoproteinemic and anti-oxidant activities of Anthocephalus indicus root extract in alloxan-induced (150 mg/kg body wt.) diabetic rats. A marked increase in plasma levels of glucose and lipid peroxides accompanied with an elevation in the lipids and apoprotein levels of serum very low density lipoprotein (VLDL) and low density lipoprotein (LDL) following decrease in lipid and protein constituents of high density lipoprotein (HDL) were observed. The alterations in lipoprotein pattern was associated with inhibition of lipolytic and antioxidant enzymes. Oral administration of root extract (500 mg/kg body wt.) for 30 days in dyslipidemic animals resulted in significant decrease in plasma glucose, total cholesterol, phospholipids, triglyceride and lipid peroxides. The decrease of lipids and apoprotein levels of VLDL and LDL were followed by stimulation of plasma post-heparin lipolytic activity and lecithin cholesterol acyltransferase as well as hepatic superoxide dismutase and catalase activities. Lipid and apoprotein levels of HDL were also recovered partially on treatment with root extract.
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Objective: To explore lipid peroxidation injuries of pancreatic mitochondria and lysosome following severe acute pancreatitis (SAP) and the protective effects of gardenia jasminoides ellis (GJE) thereof. Methods: SAP models were induced by retrograde injection of 1.5% sodium deoxycholate. The rats were randomly divided into three groups: sham group, SAP group and GJE group. The changes were measured in superoxide dismutase (SOD), malondialdehyde (MDA), membrane fluidity of mitochondria and lysosome in pancreas and succinic dehydrogenase (SDH) in mitochondria, acid phosphatase (ACP) in lysosome.The effects of GJE were also observed. Results: Compared with Sham group, the activity of SOD and membrane fluidity of mitochondria and lysosome were decreased in pancreas, and the content of MDA were increased; the releasing rate of ACP was significantly higher in lysosome; SDH in mitochondria was lower in SAP group(P < 0.01). The above-mentioned indexes were obviously ameliorated in GJE group than those in SAP group(P < 0.01). The correlation analysis indicated that MDA was negatively correlated with SOD, positively correlated with membrane fluidity (P < 0.01). Conclusion: GJE can alleviate lipid peroxidation by getting rid of oxygen free radicals of pancreatic subcellular fraction in the course of SAP, and protect the structure and function of pancreatic subcellular fraction.
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Cadmium (Cd), is an environmental and industrial pollutant that affects the male reproductive system. Cd induces its effect by affecting tissue antioxidant enzyme systems. Green tea extract (GTE) is an antioxidant and free radicals scavenger and has a chelating property. The purpose of this study was to investigate the protective effect of GTE against testes damage induced by Cd. Four groups of male rats, were utilized as following: Controls, GTE treated, Cd treated and Cd + GTE, treated rats at the same doses. The rats received GTE and or Cd orally in drinking water. After 5 weeks, the animals were sacrificed and testes were removed for microscopic and Biochemical evaluation. The levels of lipid peroxides (LPO) and glutathione (GSH) were detected in the tissue homogenates of rat testes. The current study showed marked morphological changes in the form of swelling, congestion, hemorrhage and necrosis in testes of rats treated with Cd alone. However, the rats treated with Cd+GTE showed milder edema, congestion and minute foci of necrosis in the testes. The LPO levels were significantly higher as compared to control and of GSH were significantly lower in Cd-treated rats but when GTE was co-administrated with Cd, there was an effective reduction in oxidative stress as shown by a significant rise of GSH level. In conclusion, the rats received GTE + Cd could enhance antioxidant/ detoxification system which consequently reduced the oxidative stress in rat testes. The beneficial effect of GTE is thus potentially reducing Cd toxicity and tissue damage.
El cadmio (Cd), es un contaminante del medio ambiente e industrial que afecta al sistema reproductivo masculino. Cd induce su efecto por afección de los sistemas enzimáticos antioxidantes de los tejidos. El extracto de té verde (ETV) es un antioxidante y buscador de radicales libres y tiene una propiedad quelante. El objetivo de este estudio fue investigar el efecto protector de ETV contra daños provocado por Cd a los testículos. Cuatro grupos de ratas macho, se utilizaron: Controles, tratados con ETV, tratados con Cd y tratados con Cd + ETV, todas las ratas tratadas con las mismas dosis. Las ratas recibieron ETV o Cd por vía oral en el agua potable. Después de 5 semanas, los animales fueron sacrificados y los testículos fueron retirados para la evaluación microscópica y bioquímica. Los niveles de peróxidos lípidos (LPO) y de glutation (GSH) fueron detectados en el tejido homogenizado de rata testículos. El estudio demostró marcados cambios morfológicos como inflamación, congestión, hemorragia y necrosis en los testículos de las ratas tratadas solamente con Cd. Sin embargo, las ratas tratadas con Cd + ETV mostraron leves signos de edema, congestión y focos de necrosis en los testículos. Los niveles de LPO fueron significativamente mayores en comparación con el control y la de GSH fue significativamente menor en las ratas tratadas con Cd, pero cuando ETV fue co-administrado con Cd, hubo una reducción efectiva en el estrés oxidativo, como lo demuestra el aumento significativo del nivel de GSH. En conclusión, las ratas recibieron GTE + Cd que podría aumentar el sistema antioxidante / desintoxicación, por tanto, reducir el estrés oxidativo en los testículos de ratas. El efecto beneficioso de GTE es reducir la toxicidad y el daño tisular causado Cd.
Subject(s)
Animals , Male , Rats , Cadmium/toxicity , Oxidative Stress , Plant Extracts/pharmacology , Tea , Testis , Testis/pathology , Antioxidants/pharmacology , Glutathione/metabolism , Lipid Peroxides/metabolism , Rats, Sprague-DawleyABSTRACT
To study antioxidant role of zinc, the effects of dietary zinc deficiency and vitamin E supplementation on lipid peroxidation were studied. Levels of zinc and vitamin E in blood and liver were also measured. Forty Sprague-Dawley male rats aging 8 weeks old were used as experimental animals. Zinc deficient diet (Zn, 0 ppm), zinc normal diet (Zn, 36.5 ppm), and vitamin E supplemented diet (1,000 IU alpha-tocopherol/kg of diet) were used as experimental diet. During the first three weeks, rats were divided into zinc normal (ZnN, 8 animals) and zinc deficient (ZnD, 32 animals) group. Eight rats from each group were sacrificed to get blood and liver after 3 weeks of experiment. The remaining 24 zinc deficient rat were then divided into zinc normal (ZnDN), zinc deficient (ZnDD), vitamin E supplemented (ZnDE) diet groups. After another 3 weeks of experiment, all animals were sacrificed as well. Thiobarbituric acid reactive substance (TBARS) levels in plasma and liver, conjugated diene levels in liver were measured as lipid peroxidation index. There were no significant differences in food intake, body weight gain, and food efficiency ratio among groups. Weights of liver per 100 g body weight were not significantly different. There were no significant differences in Zn levels in serum. Plasma and liver TBARS level, and liver conjugated diene level were significantly lower in ZnDE than in ZnDN or ZnDD, and significantly higher in ZnDD than in ZnDN. Therefore, it seems that lipid peroxidation is accelerated by dietary zinc deficiency and recovered partly by vitamin E supplementation.
Subject(s)
Animals , Humans , Male , Rats , Aging , Body Weight , Diet , Eating , Lipid Peroxidation , Lipid Peroxides , Liver , Plasma , Thiobarbiturates , Thiobarbituric Acid Reactive Substances , Vitamin E , Vitamins , Weights and Measures , ZincABSTRACT
Objective To investigate effects of ginkgo biloba extract(GBE) and tanshinoneⅡ A preventative administration against cerebral ischemia and reperfusion injury in gerbils.Methods Cerebral iscthemia and reperfu- sion injury were made by 10 minutes'occlusion of bilateral carotid arteries followed by 24 hours' reperfusion in ger- bils.GBE,tanshinone Ⅱ A,nimodipine or GBE plus tanshinone Ⅱ A were administrated intragastrically 3 days prior to and at the day of ischemia and reperfusion.Effects of experimental agents on mortality,stroke index,brain body index,water content in brain hemisphere,level of SOD activity and MDA in cerebral tissue were measured,and pathological changes of cortex and hippoearnpal CA1 sector were observed.Results GBE 48 mg/kg and tanshinone Ⅱ A 25mg/kg preventive administration could significantly reduce the stroke index,brain body index,and water in brain hemisphere,together with a reduced mortality of cerebral ischemia and reperfusion injuried gerbils.The two a- gents could also significantly improve the activity of SOD,reduce the level of MDA in cerebral tissue and the injury in cortex and hippocampal CA1 sector.Moreover,combined treatment of these two agents demonstrated more signifi- cant effects.Conclusion GBE,tanshinone Ⅱ A and combined therapy of these two agents may protect cerebral func- tion from ischemia and reperfusion injury through reducing the cerebral edema and attenuating the injury of oxygen free radicals.
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A cross-sectional study was done to see the possible association of plasma lipid peroxides in the elderly with age and other factors. Plasma lipid peroxides is a product of free radical reactions which according to the latest theory of aging is the cause of aging process. Lipid peroxides were also found high in coronary heart disease. Four hundred forty relatively healthy elderly, age 55-85 years, were randomly chosen from free living elderly under guidance of health care centers (PUSKESMAS) in Jakarta. Anamnesis and physical examination were done in the morning in the health centers. Blood samples were taken in fasting conditions, plasma lipids and lipid peroxides were measured according to standard methods. There was an age difference of lipid peroxides level in the elderly, which increased with age up to 70 years old. Elderly 70 years old and over had low plasma lipid peroxides. The level was not related to high plasma lipids. Higher level was found when more chronic degenerative diseases were found.
Subject(s)
Aged , Lipid PeroxidesABSTRACT
This study was performed to investigate the effect of dietary beta-carotene supplementation on lipid peroxide levels and antioxidant enzyme activities in alcoholic fatty liver rats. Forty five Sprague-Dawley male rats aging 8 weeks were used as experimental animals, which were divided into the control diet (CD) and the ethanol diet (ED) and the ethanol + 0.02% beta-carotene diet (EbetaD) groups and fed the experimental diet respectively for 5 weeks. After the feeding, rats were sacrificed to get blood and liver to analyze lipid and lipid peroxide levels and antioxidant enzyme activities. The mean body weight and food intake of the ethanol diet group was significantly lower than that of the control diet. The liver index (LI) of the ethanol diet group was significantly higher than those of the control diet and the beta-carotene supplementation group. Serum levels of total lipid, triglyceride of the ethanol diet group were significantly higher than those of the control diet and the beta-carotene supplementation group. Total cholesterol levels were not significantly different among all groups. HDL-cholesterol of the ethanol diet group was significantly lower than those of the control diet and the beta-carotene supplementation group. Liver TBARS of the ethanol diet group was significantly higher than those of the control diet and the beta-carotene supplementation group. Liver lipofuscin and conjugated diene levels were not significantly different among all groups. The superoxide dismutase activity of the ethanol diet group was significantly lower than those of the control diet and the beta-carotene supplementation group. Catalase and glutathione peroxidase activities were not significantly different among all groups. Because beta-carotene supplementation significantly decrease the serum total lipid, triglyceride, liver TBARS levels and increase the superoxide dismutase activity in alcoholic fatty liver rats, beta-carotene supplementation seems to give beneficial effect for the alcoholics.
Subject(s)
Animals , Humans , Male , Rats , Aging , Alcoholics , beta Carotene , Body Weight , Catalase , Cholesterol , Diet , Eating , Ethanol , Fatty Liver , Fatty Liver, Alcoholic , Glutathione Peroxidase , Lipid Peroxides , Lipofuscin , Liver , Rats, Sprague-Dawley , Superoxide Dismutase , Thiobarbituric Acid Reactive Substances , TriglyceridesABSTRACT
This study investigated the effect of dietary beta-carotene supplementation on lipid peroxidation and anti oxidative enzyme activity as indices of oxidative stress in diabetic rats. Fifty Sprague-Dawley male rats aging 7 weeks were used as experimental animals, which were divided into the non-diabetic control group and the diabetic group. The diabetic group received an intraperitoneal injection with streptozotocin to induce diabetes. Then the diabetic rats were divided into four dietary groups which contained different amounts of beta-carotene; 0%, 0.002%, 0.02%, or 0.2% of the diet. The diabetic rats were fed the experimental diets and the non-diabetic rats were fed the basal diet without beta-carotene supplementation for 2 weeks and then sacrificed. The diabetic group had a significantly higher blood glucose level than the non-diabetic group. However, blood glucose level were not significantly changed by the level of dietary beta-carotene supplementation. Compared to the non-diabetic control group, the diabetic control group indicated a significant increase of plasma thiobarbituric acid reactive substance (TBARS). Liver TBARS level also tended to be higher in diabetic control group, although it was not significant. The beta-carotene supplementation did not reduce plasma TBARS level. However, Liver TBARS level was significantly decreased when 0.02% or more beta-carotene was supplemented in the diet. The liver lipofuscin level in the diabetic control group was higher than in the non-diabetic control group, but the effect of beta-carotene supplementation did not show any differences. Superoxide dismutase activity was significantly lower in the diabetic group, but it was increased in groups receiving 0.02% or more beta-carotene. Compared to the non-diabetic control group, lower activities of catalase and glutathione peroxidase were observed in the diabetic control group, although it was not significant. Catalase and glutathione peroxidase activities tended to increase as the levels of beta-carotene supplementation increased, although it was not statistically significant. Therefore, it seems that dietary beta-carotene supplementation might reduce diabetic complications by partly decreasing the lipid peroxidation and increasing the activity of antioxidative enzyme in diabetes.
Subject(s)
Animals , Humans , Male , Rats , Aging , beta Carotene , Blood Glucose , Catalase , Diabetes Complications , Diet , Glutathione Peroxidase , Injections, Intraperitoneal , Lipid Peroxidation , Lipid Peroxides , Lipofuscin , Liver , Oxidative Stress , Plasma , Rats, Sprague-Dawley , Streptozocin , Superoxide Dismutase , Thiobarbituric Acid Reactive SubstancesABSTRACT
The purpose of this study was to observe the effects of dietary intervention, through the modification of dietary fatty acids composition and antioxidant vitamins, on plasma thromboxane B2 (TXB2) levels in postmenopausal women with hypercholesterolemia. The subjects were treated for 12 weeks with one of three methods: hormone replacement therapy (HRT group, n=8), dietary intervention (DIET group, n=8), or HRT combined with dietary intervention (HRT +DIET group, n=8). Changes in serum phospholipid fatty acids composition, serum peroxides, and plasma TXB2 levels were measured at weeks 0, 4 and 12. The P/S ratio increased and the n-6/ n-3 ratio decreased in the DIET and the HRT +DIET group at week 4 (p<0.05). The ratio of C20:5/C20:4 in serum phospholipid increased in the DIET (p<0.05) and the HRT +DIET groups (NS) at week 4. Plasma TXB2 levels decreased in the DIET (-35%, p<0.05) and the HRT +DIET groups (-18.8%, NS) at week 4. Serum lipid peroxides levels significantly decreased by 10.5% and 15.2% in the DIET group at weeks 4 and 12, and by 10.8% in the HRT +DIET group only at week 12 (p<0.05). Dietary intervention may lower thrombotic risks in Korean postmenopausal women by changing the serum fatty acid composition, serum lipid peroxides levels and plasma thromboxane B2 levels.