Lipidomic investigation of the protective effects of Polygonum perfoliatum against chemical liver injury in mice / 中西医结合学报

OBJECTIVE@#Recent investigations have demonstrated that Polygonum perfoliatum L. can protect against chemical liver injury, but the mechanism behind its efficacy is still unclear. Therefore, we studied the pharmacological mechanism at work in P. perfoliatum protection against chemical liver injury.@*METHODS@#To evaluate the activity of P. perfoliatum against chemical liver injury, levels of alanine transaminase, lactic dehydrogenase, aspartate transaminase, superoxide dismutase, glutathione peroxidase and malondialdehyde were measured, alongside histological assessments of the liver, heart and kidney tissue. A nontargeted lipidomics strategy based on ultra-performance liquid chromatography quadrupole-orbitrap high-resolution mass spectrometry method was used to obtain the lipid profiles of mice with chemical liver injury and following treatment with P. perfoliatum; these profiles were used to understand the possible mechanisms behind P. perfoliatum's protective activity.@*RESULTS@#Lipidomic studies indicated that P. perfoliatum protected against chemical liver injury, and the results were consistent between histological and physiological analyses. By comparing the profiles of liver lipids in model and control mice, we found that the levels of 89 lipids were significantly changed. In animals receiving P. perfoliatum treatment, the levels of 8 lipids were significantly improved, relative to the model animals. The results showed that P. perfoliatum extract could effectively reverse the chemical liver injury and significantly improve the abnormal liver lipid metabolism of mice with chemical liver injury, especially glycerophospholipid metabolism.@*CONCLUSION@#Regulation of enzyme activity related to the glycerophospholipid metabolism pathway may be involved in the mechanism of P. perfoliatum's protection against liver injury. Please cite this article as: Peng L, Chen HG, Zhou X. Lipidomic investigation of the protective effects of Polygonum perfoliatum against chemical liver injury in mice. J Integr Med. 2023; 21(3): 289-301.

Efectividad del Vimang® en pacientes con lesión hepática a causa del virus del dengue / Effectiveness of the Vimang® in patients with liver damage due to dengue virus

Introducción: En la evolución de la infección por el virus de dengue es frecuente la aparición de la lesión hepática, lo cual se asocia con el estrés oxidativo. Objetivo: Demostrar la efectividad del concentrado de Vimang® en pacientes con diagnóstico de lesión hepática por virus del dengue. Métodos: Se efectuó un ensayo clínico en fase III, abierto y aleatorizado, en la consulta de Hepatología del Hospital Provincial Docente Clinicoquirúrgico Saturnino Lora Torres de Santiago de Cuba, desde junio del 2014 hasta igual mes del 2017, consistente en la aplicación del concentrado de Vimang® en 39 pacientes con hepatitis reactiva por dengue, que conformaron el grupo de estudio, para luego comparar los resultados con los del grupo de control, integrado por igual número de pacientes con la afección, en quienes solo se aplicaron las medidas higiénico-dietéticas habituales. Resultados: En la serie se obtuvo un descenso importante de los valores medios de las pruebas para evaluar la función hepática en ambos grupos de trabajo, pero fueron más significativos en los pacientes que recibieron Vimang®. Del mismo modo, a los 9 meses se apreció una mejoría en 89,0 por ciento de los casos en cuanto a la disminución de los síntomas, frente a tan solo 69,2 por ciento de los controles. La hepatomegalia, como signo físico más importante, desapareció en el total de los casos al año de seguimiento clínico; sin embargo, se mantuvo en 7,2 por ciento del grupo de control. Conclusiones: Pudo demostrarse que el Vimang® influye de manera importante en el control de los síntomas y en la mejoría humoral de los pacientes que presentan lesión hepática ocasionada por el dengue.

Introduction: The emergence of the liver damage is frequent in the clinical course of the infection due to the dengue virus, which is associated to the oxidative stress. Objective: To demonstrate the effectiveness of the Vimang® concentrate in patients with diagnosis of liver damage due to dengue virus. Methods: A clinical open and randomized assay in phase III was carried out, in the Hepathology department of Saturnino Lora Torres Teaching Provincial Clinical Surgical Hospital in Santiago de Cuba, from June, 2014 to the same month in 2017, consistent in the use of Vimang® concentrate in 39 patients with reactive hepatitis due to dengue fever, who formed the study group, and then the results were compared with those of the control group, integrated by equally number of patients with the affection, in whom the habitual hygienic-dietary measures were applied. Results: In the series an important decrease of the mean values of the tests was obtained to evaluate the hepatic function in both groups, but they were more significant in the patients who received Vimang®. In the same way, an improvement was appreciated after 9 months in 89.0 percent of the cases as for the decrease of the symptoms, compared to a 69.2 percent of the controls. Hepatomegaly, as the most important physical sign, disappeared in the total of the cases after a year of clinical follow-up; however, it remained in 7.2 percent of the control group. Conclusions: It could be demonstrated that Vimang® influences in a significant way in the control of the symptoms and in the humoral improvement of the patients who present liver damage caused by dengue fever.

Can thiamine pyrophosphate prevent desflurane induced hepatotoxicity in rats?

ABSTRACT PURPOSE : To investigate the effects of thiamine pyrophosphate (TPP) against desflurane induced hepatotoxicity. METHODS : Thirty experimental animals were divided into groups as healthy (HG), desflurane control (DCG) , TPP and desflurane group (TDG). 20 mg/kg TPP was injected to intraperitoneally TDG. After one hour of TPP administration, desflurane was applied for two hours. After 24 hours, liver tissues of the animals killed with decapitation were removed. The oxidant/antioxidant levels and ALT, AST and LDH activities were measured. The histopathological examinations were performed in the liver tissues for all rats. RESULTS : Notwithstanding the levels of oxidants and liver enzymes were significantly increased (p<0.0001), antioxidant levels were significantly decreased in DCG (p<0.0001). On contrary to the antioxidant parameters were increased (p<0.05) the oxidant parameters and liver enzymes were decreased in TDG (p<0.0001). Whereas multiple prominent, congestion, hemorrhage and dilatation were observed in sinusoids and lymphocyte-rich inflammation results in the centrilobular and portal areas of liver tissue in DCG, these findings were observed less frequently in TDG. CONCLUSİON : Thiamine pyrophosphate prevented liver oxidative damage induced with desflurane and may be useful in prophylaxis of desflurane induced hepatotoxicity.

Cytotoxicity and hepatoprotective attributes of methanolic extract of Rumex vesicarius L

BACKGROUND: To evaluate the hepatoprotective potential and invitro cytotoxicity studies of whole plant methanol extract of Rumex vesicarius L. Methanol extract at a dose of 100 mg/kg bw and 200 mg/kg bw were assessed for its hepatoprotective potential against CCl4-induced hepatotoxicity by monitoring activity levels of SGOT (Serum glutamic oxaloacetic transaminase), SGPT (Serum glutamic pyruvic transaminase), ALP (Alkaline phosphatase), TP (Total protein), TB (Total bilirubin) and SOD (Superoxide dismutase), CAT (Catalase), MDA (Malondialdehyde). The cytotoxicity of the same extract on HepG2 cell lines were also assessed using MTT assay method at the concentration of 62.5, 125, 250, 500 µg/ml. RESULTS: Pretreatment of animals with whole plant methanol extracts of Rumex vesicarius L. significantly reduced the liver damage and the symptoms of liver injury by restoration of architecture of liver. The biochemical parameters in serum also improved in treated groups compared to the control and standard (silymarin) groups. Histopathological investigation further corroborated these biochemical observations. The cytotoxicity results indicated that the plant extract which were inhibitory to the proliferation of HepG2 cell line with IC50 value of 563.33 ± 0.8 Mg/ml were not cytotoxic and appears to be safe. CONCLUSIONS: Rumex vesicarius L. whole plant methanol extract exhibit hepatoprotective activity. However the cytotoxicity in HepG2 is inexplicable and warrants further study.

Attenuation of copaiba oil in hepatic damage in rats

PURPOSE: To investigate the copaiba oil on the hepatic damage induced by acetaminophen, comparing against corn oil. METHODS: Fifty four rats were distributed into nine study groups (N=6): control group, that didn't receive the acetaminophen; Acetaminophen Group, that only received the acetaminophen; Prophylactic Copaiba Group 1, that received copaiba oil two hours before the acetaminophen; Prophylactic Copaiba Group 7, that received copaiba oil seven days, once by day, before the acetaminophen; Therapy Copaiba Group, that received the copaiba oil two hours after the acetaminophen, the corn's groups were similar than copaiba oil groups; and N-Acetyl-Cysteine Group, that received the N-Acetyl-Cysteine two hours after the acetaminophen. Euthanasia was performed after 24 hours. The serum levels transaminases, bilirubin and canalicular enzymes were analyzed. RESULTS: The prophylactic copaiba group 7, therapy copaiba group and N-Acetyl-Cysteine Group showed amounts of AST and ALT similar to the control group; and the prophylactic copaiba group 1 and corn's groups showed similar levels to the acetaminophen group. There was no significant difference between the groups regarding the amount of alkaline phosphatase and ɤ GT (p>0.05). The therapy copaiba group showed the highest levels of total bilirubin and was statistically different from the other groups (p<0.01). CONCLUSIONS: Copaiba oil administered prophylactically for seven days and therapeutically 2 hours after the acetaminophen acute intoxication offered a potential hepato protection against paracetamol-induced hepatic damage, normalizing the biochemical parameters similarly to N-Acetyl-Cysteine, and the treatment with corn oil shows no effect on the liver damage. .

Antioxidant potential of different grape cultivars against Fenton-like reagent-induced liver damage ex-vivo.

The phytochemicals present in the grapes are responsible for nutraceutical and health benfits due to their antioxidant properties. These phytochemicals, however, vary greatly among different cultivars. In this study, we evaluated the antioxidant potential and protective role of four different Indian grape (Vitis vinifera) cultivars extracts, namely Flame seedless (Black grapes), Kishmish chorni (Black with reddish brown), Red globe (Red) and Thompson seedless mutant (Sonaka, Green) against the Fenton-like reagent (200 mmole H2O2, 2 mmole ascorbate, 25 mmole FeSO4)-induced liver damage. Non-enzymatic antioxidants, such as glutathione (GSH) levels and activities of antioxidant enzymes, such as glutathione S-transferase (GST) and superoxide dismutase (SOD), as well as total antioxidant capacity (TAC) were highest in the grape seed, followed by skin and pulp. Among edible parts of different cultivars, skin of Flame seedless (Black) cultivar showed highest antioxidant potential, while the Thompson seedless the least potential. These antioxidants were found to be significantly (P<0.01) correlated with the levels of total phenol, flavonoids and ascorbic acid. Fenton-like reagent treatment significantly (P<0.001) decreased GSH content by 39.1% and activities of catalase (CAT) by 43.2% and glutathione reductase (GR) by 60%, while increasing thiobarbituric acid reactive substances (TBARS) and nitric oxide levels by 2.13-fold and 0.64-fold, respectively and GST activity by 0.81-fold. Pre-treatment with grape seed extracts showed the best hepatoprotective action against Fenton-like reagent-induced damage, followed by the extracts of skin and pulp of any cultivar. Thus, our study showed the significant amounts of antioxidants were in grape seed, followed by its skin and pulp, which varied among the cultivars and was associated with the protective action of grape extracts against Fenton-like reagent-induced liver damage ex-vivo.

Protective effect of bixin on carbon tetrachloride-induced hepatotoxicity in rats

BACKGROUND: The liver is an important organ for its ability to transform xenobiotics, making the liver tissue a prime target for toxic substances. The carotenoid bixin present in annatto is an antioxidant that can protect cells and tissues against the deleterious effects of free radicals. In this study, we evaluated the protective effect of bixin on liver damage induced by carbon tetrachloride (CCl4) in rats. RESULTS: The animals were divided into four groups with six rats in each group. CCl4 (0.125 mL kg-1 body wt.) was injected intraperitoneally, and bixin (5.0 mg kg-1 body wt.) was given by gavage 7 days before the CCl4 injection. Bixin prevented the liver damage caused by CCl4, as noted by the significant decrease in serum aminotransferases release. Bixin protected the liver against the oxidizing effects of CCl4 by preventing a decrease in glutathione reductase activity and the levels of reduced glutathione and NADPH. The peroxidation of membrane lipids and histopathological damage of the liver was significantly prevented by bixin treatment. CONCLUSION: Therefore, we can conclude that the protective effect of bixin against hepatotoxicity induced by CCl4 is related to the antioxidant activity of the compound.

Thymoquinone supplementation ameliorates acute endotoxemia-induced liver dysfunction in rats

Endotoxemia caused by lipopolysaccharide [LPS] produced an inflammatory condition contributing to multiple organ failure. This study was carried out to investigate the effects of thymoquinone [TQ], the main constituent of Nigella saliva seeds, against LPS-induced hepatotoxicity. The obtained data revealed that LPS markedly depleted liver reduced glutathione [GSH] and significantly increased the level of malondialdehyde [MDA] and the activity of caspase-3 enzyme in the liver. Serum tumour necrosis factor-alpha [TNF-alpha] and bilirubin levels and the activities of alkaline phosphatase [ALP] and gamma-glutamyl transferase [gamma-GT] enzymes were markedly increased in LPS-treated rats. TQ supplementation resulted in normalization of liver GSH and decreases in the levels of MDA and caspase-3 activity in the liver with reduction of serum TNF-alpha, serum total bilirubin and the actvities of ALP and gamma-GTenzymes. Histopathological examination revealed that TQ administration improved LPS-induced pathological abnormalities in liver tissues. The present study conclude that TQ reduced acute endoxemia-induced liver dysfunction at least in part by its anti-inflammatory, antiapoptotic and antioxidant activities

Hepato and reno protective action of Calendula officinalis L. flower extract.

Flower extract of C. officinalis L. was evaluated for its protective effect against CCl4 induced acute hepatotoxicity and cisplatin induced nephrotoxicity. The activities of serum marker enzymes of liver injury like glutamate pyruvate transaminase (SGPT), glutamate oxaloacetate transaminase (SGOT) and alkaline phosphatase (ALP) which were increased by CCl4 injection was found to be significantly reduced by the pretreatment of the flower extract at 100 and 250 mg/kg body weight. The lipid peroxidation in liver, the marker of membrane damage and the total bilirubin content in serum were also found to be at significantly low level in the extract pretreated group, indicating its protective role. The kidney function markers like urea and creatinine were significantly increased in cisplatin treated animals. However, their levels were found to be lowered in the extract pretreated groups (100 and 250 mg/kg body weight). Moreover, cisplatin induced myelosuppression was ameliorated by the extract pretreatment. Treatment with the extract produced enhancement of antioxidant enzymes--superoxide dismutase and catalase and glutathione. Results suggest a protective role of the flower extract of C. officinalis against CCl4 induced acute hepatotoxicity and cisplatin induced nephrotoxicity. Extract has been found to contain several carotenoids of which lutein, zeaxanthin and lycopene predominates. Possible mechanism of action of the flower extract may be due to its antioxidant activity and reduction of oxygen radicals.

Hepatotoxicidade da cianotoxina microcistina / Hepatotoxicity of the microcystin cyanotoxin

Constitui interesse emergente em saúde pública avaliar a possibilidade de intoxicação humana por biotoxinas de algas cianofíceas, principalmente as hepatotoxinas do grupo das microcistinas. A microcistina, um heptapeptídeo monocíclico, é produzida principalmente pela cianobactéria Microcistis aeruginosa. São caracterizadas por alguns aminoácidos variáveis, dois deles com uma estrutura não usual que possuem importante papel na hepatotoxidade da microcistina. Apesar do acometimento humano atribuído as microcistinas incluírem gastroenterite, reações alérgicas ou irritativas, neurotoxicidade, o principal alvo da toxina é o fígado. Nos hepatócitos as microcistinas são carreadas pelo sistema transportador do ácido biliar, inibindo a atividade da proteína fosfatase no citoplasma. A inibição leva a mudanças morfológicas na membrana plasmática pela hiperfosforilação de citoqueratinas, e à atividade de promoção tumoral pelas proteínas hiperfosforiladas. Os métodos de detecção e quantificação de microcistinas no ambiente incluem a cromatografia líquida, o bioensaio em camundongos e os testes imunoenzimáticos. O último vem ganhando destaque pela praticidade e alta sensibilidade.

At public health, there is increasingly interest on evaluating the possibility of human intoxication by biotoxins from blue-green algae, mainly the hepatotoxins from the microcystin group. Microcystin, a monocyclic heptapeptide, is mainly produced by a cyanobacteria called Microcistis aeruginosa. It is characterized by a few variable amino acids, from which two of them have an unusual structure and play an important role in the hepatotoxicity of the microcystin. Although human illnesses include gastroenteritis, allergic or irritative reactions, and neurotoxicity, the main target of this toxin is the liver. Inside the hepatocytes, microcystins are carried by the transportation system of the bile acid, inhibiting the activity of the protein phosphatase in the cytoplasm. This inhibition causes a morphologic change in the plasmatic membrane because of the hyperphosphorylation of cytokeratins, and also the tumoral promotion by the hyperphosphorylated proteins. The techniques used in the detection and quantification of the microcystins in the environment include liquid chromatography, bioanalysis of mice, and immunoenzymatic tests using mono and polyclonal antibodies against those toxins. The latter has been remarked because of its practicality and its high sensibility.

Hepatobiliary clearance of labelled mebrofenin in normal and D-galactosamine HCl-induced hepatitis rats and the protective effect of turmeric extract.

This study was carried out to see the hepatobiliary clearance of 99m Tc-Mebrofenin radiopharmaceutical in D-galactosamine induced hepatic rats. Furthermore, protective effect of turmeric extract has been studied in these hepatitis rats. Hepatitis was induced with intraperitoneal injection of D-galactosamine (400 mg/kg b. wt) in these rats. 1% turmeric extract was given along with their normal diet for 15 days. Turmeric extract treatment significantly increased the hepatic uptake of radioactivity and accelerated the excretion of 99m Tc-Mebrofenin as compared to control rats. (P < 0.001). In D-galactosamine administered rats, a significant delay was observed in 99m Tc-Mebrofenin excretion as compared to controls. However, D-galactosamine administered rats, pretreated with turmeric extract or concurrently treated with turmeric extract showed a near normal pattern of 99m Tc-Mebrofenin excretion. Hence, it can be suggested that turmeric extract may improve the liver function by detoxification.

Effect of propriety herbal formulation against chronic carbon tetrachloride induced hepatotoxicity.

Efficacy of propriety herbal formulation (PHF) against carbon tetrachloride (CCl4) induced liver damage was investigated in adult rats. Administration of CCl4 (0.2 ml/kg; i.p.) twice a week for 12 weeks resulted in significant elevation in serum transaminases activity. Level of reduced glutathione was significantly decreased. On the contrary, significant elevation was found in the hepatic lipid peroxidation level. Proliferation of fibroblast replaced the hepatic parenchyma cells in focal areas. Cell organelles like mitochondria, endoplasmic reticulum and nucleus showed severe degeneration after CCl4 exposure. PHF was effective in restoring the CCl4 induced biochemical and histological ultrastructural changes.

Hepatoprotective action of abhrak bhasma, an ayurvedic drug in albino rats against hepatitis induced by CCl4.

Abhrak bhasma is a commonly used ayurvedic drug against many diseases including hepatitis. It is tested in albino rats using a model of hepatitis induced by a single dose of CCl4 (3 ml/kg body wt). Different doses of abhrak bhasma (10, 20, 30 and 40 mg/kg body wt) were tested to decide the dose related hepatoprotective efficacy. The centrolobular necrosis induced by single dose of CCl4 was reduced significantly by abhrak bhasma (10 mg) and liver histology was also protected by 20 mg dose. Liver acid lipase activity was lowered, while alkaline and lipoprotein lipase activities were elevated due to treatment of single dose of CCl4. Abhrak bhasma counteracted the action of CCl4 on liver lipolytic enzymes. CCl4 did not alter the kidney histologically. Activities of three lipases of rat kidney (acid, alkaline and lipoprotein lipases) were reduced by CCl4 treatment and were reversed by administration of abhrak bhasma. Acid lipase activity of rat adipose tissue was reduced by CCl4 treatment. On the contrary alkaline, lipoprotein and hormone sensitive lipases were enhanced after 24 hr of administration of CCl4. Acid lipase activity was raised by administration of different doses of abhrak bhasma concurrent with CCl4. Abhrak bhasma treatment along with CCl4 enhanced alkaline lipase activity at 10 and 20 mg dose and later it was reduced at 30 and 40 mg doses and came to normal levels. Lipoprotein and hormone sensitive lipases were reduced by the counteraction of increasing doses of abhrak bhasma.

Effect of Indigofera tinctoria Linn on liver antioxidant defense system during D-galactosamine/endotoxin-induced acute hepatitis in rodents.

Effects of pre-treatment with the alcoholic extract of I. tinctoria (500 mg/kg body wt/day, p.o. for 21 days) on liver antioxidant defense system during acute hepatitis induced by D-galactosamine (D-GalN)/endotoxin (LPS extracted by phenol water method from E. coli serotype 0111.B4; 300 mg and 30 micrograms/kg body wt/day, i.p., 18 hr before the assay) were investigated on the activities of enzymic antioxidants such as superoxide dismutase, catalase, glutathione peroxidase and glutathione-s-transferase, and levels of total reduced glutathione in the liver of normal and experimental groups of male albino rats. Since lipid peroxidation and associated membrane damage is a key feature of D-galN/LPS-induced liver injury, the levels of lipid peroxides, was estimated and used as an index of oxidative stress. D-GalN/endotoxin-induced hepatic damage was manifested by a significant decrease in the activities of antioxidant enzymes, decreased glutathione levels and increased levels of lipid peroxides. I. tinctoria pre-treated rats showed considerable protection against D-galN/endotoxin, induced oxidative stress as evidenced by a significant increase in the activities of all the antioxidant enzymes studied and significant decrease in the levels of lipid peroxides. Results indicate that pretreatment with I. tinctoria extract in rats is very effective in reducing D-GalN/endotoxin-induced oxidative stress suggesting an antioxidant effect.

Effect of HD-03--a herbal formulation in galactosamine-induced hepatopathy in rats.

The effect of HD-03 a herbal preparation was studied on galactosamine (400 mg/kg b.wt., i.p.) induced hepatotoxicity in rats. Animals were pre-treated for 14 days with HD-03 and compared against untreated group for SGPT, SGOT, serum bilirubin and liver glycogen. Histopathology of liver lobes was considered to evaluate the extent of hepatic injury induced by galactosamine. These were reversed by HD-03 pre-treatment. HD-03 provided convincing evidence of hepatoprotection against galactosamine induced hapatotoxicity.

Protection of CCL4-induced liver damage in rats by some calcium channel blockers.

Liver necrosis was produced in rats by administering 3 doses o a mixture o carbon tetrachloide+olive oil, 2 ml/kg, ip. The liver damage was evidenced by the elevated levels serun aspartate aminotrans ferase (AST), alanine aminotransferase (AIT) and gamma glutamyl transpeptidase (gamma-GT) and by histopathological observations of liver sections. Nitrendipine, nimodipine and nisoldipine (1 mg/100 g of rat, ip) significantly reduced these elevated levels of AST, AIT and gamma-GT. Carbon tetrachloride induced liver necrosis was also found to be significantly reduced in nitrendipine, nimodipine and nisoldipine pre-treated animals as observed macroscopically and histologically.

Anti tubercular treatment induced hepatotoxicity: does acetylator status matter?

Anti tubercular drug related hepatotoxicity is common. The mechanism of injury and factors predisposing to its development are not fully understood. Forty patients with anti tubercular drugs related hepatotoxicity were studied to see the clinical and biochemical profile of these patients and to find out the significance of acetylator phenotype in the development of hepatotoxicity. Mean age of patients with liver damage (37.82 +/- 10.0 years) was similar to those without liver damage (36.48 +/- 12.5 years). Pyrazinamide appeared to increase the hepatotoxicity of isoniazid and rifampicin. The percentage of rapid acetylators and slow acetylators among patients with hepatotoxicity (70% and 30% respectively) was similar to controls (66.6% rapid and 33.3% slow acetylators). Acetylator phenotype probably has no role in anti tubercular drugs induced hepatotoxicity.

Down regulation of tumour necrosis factor activity in experimental hepatitis by a herbal formulation, Liv. 52.

A herbal hepatoprotective formulation Liv 52 down regulated the tumour necrosis factor (TNF) production in Charles Foster Rats treated with CCl4. Inhibition of TNF activity was proportional to the hepatoprotective activity.

Hepato protective effect of Liv-52 against CCl4 induced lipid peroxidation in liver of rats.

Effect of oral feeding of Liv-52, on lipid peroxidation in normal liver and damaged liver induced by CCl4 of albino rats was studied. While Liv-52 did not show any effect on normal healthy liver cells, it had a significant protective effect against damage by CCl4 as shown by significant decrease in malonaldialdehyde content.

Investigacion sobre toxicidad hepatica de medicacion antituberculosa / Study of the hepatic toxicity of antituberculouis drugs treatment

El presente trabajo fue realizado en el hospital San Gabriel entre enero a marzo de 1990, con 47 pacientes que fueron estudiados durante su tratamiento en diferentes etapas, y muestra el grado de tolerancia hepatica a medicamentos que deben ser utilizados por largo tiempo y que de acuerdo a reaccion individual es imprevisible el grado de toxicidad que pueda esperarse. Los resultados son alentadores porque no se tuvieron que lamentar grados extremos de toxicidad y solo en tres casos, la suspension temporal del tratamiento