Action of Vitamin E on Experimental Severe Acute Liver Failure

Abstract

-Background -Severe Acute Liver Failure (ALF) is a life-threatening clinical syndrome characterized by hepatocyte necrosis, loss of hepatic architecture, and impairment of liver functions. One of the main causes of ALF is hepatotoxicity from chemical agents, which damage hepatocytes and result in increase of reactive oxygen species. The vitamin E isoform is the one with the strongest biological antioxidant activity. Objective -To evaluate the antioxidant effect of vitamin E in this ALF model. Methods -We used 56 rats (mean weight of 300 g) divided into eight groups, four groups assessed at 24 hours and 4 assessed at 48 hours after induction: control group (CO); Vitamin E (Vit. E); Thioacetamide (TAA) and Thioacetamide + Vitamina E (TAA+Vit.E). Rats were submitted to injections of thioacetamide (400 mg/kg i.p.) at baseline and 8 hours later. Vitamin E (100 mg/kg ip) was administered 30 minutes after the second dose of thioacetamide. The 48-hour group rats received two additional doses of vitamin E (24h and 36h). At 24h or 48 hours after the administration of the first dose of TAA, rats were weighed and anesthetized and their blood sampled for evaluation of liver integrity through enzymes aspartate aminotransferase (AST) and alanine aminotransferase (ALT). Liver tissue was sampled for assessment of lipid peroxidation (LPO) by the technique TBARS, antioxidant enzymes SOD, CAT, GPx and GST activity, levels of the NO 2 /NO 3 and histology by H&E in two times. The results were expressed as mean ± standard deviation and statistically analyzed by ANOVA followed by Student-Newman-Keuls, with P<0.05 considered as significant. The histopathological evaluation showed a decrease in liver injury (necrosis and inflammation) in both studied times. Conclusion -These results suggest that vitamin E was able to protect the liver from lesions caused by thioacetamide. HEADINGS -Acute liver failure. Thioacetamide. Oxidative stress. Antioxidants.

Protective action of glutamine in rats with severe acute liver failure

“…We also observed an increase in TBARS levels in the livers of animals in the TAA group, which is indicative of increased lipid peroxidation. Other authors found similar increases in TBARS in studies that used TAA to induce liver damage[6,7,43]. Again, Gln administration was able to reduce these levels in our animals, corroborating the findings of several other studies that have demonstrated its protective effect in different experimental models[21,26,47].…”

“…Reactive oxygen species (ROS) are generated during the process of oxygen metabolism and play several important physiological roles, including signal transduction, defense against microbial pathogens, and gene expression to support cell growth or cell death signaling pathways[5,10]. Reactive nitrogen species (RNS), in turn, are derived from nitric oxide (NO), which is produced via inducible nitric oxide synthase (iNOS) activity[5,6]. Because of their unique chemical characteristics, ROS and RNS can trigger lipid peroxidation and cause DNA strand breaks and protein oxidation, resulting in cellular injury.…”

Hepatoprotective influence of quercetin and ellagic acid on thioacetamide-induced hepatotoxicity in rats

“…induces marked hepatic damage characterized by significant elevation liver function tests (AST, ALT and ALP) and hepatic MDA content as well as diminution of TAC and GPX enzyme activity. Those findings are consistent withTalluri et al (2016) andMiguel et al (2017) who reported that TAA induced hepatic toxicity and oxidative damage in rats. The liver enzymes are the most frequently diagnostic markers for liver cell damage and necrosis(Thapa and Walia 2007).Reduction in the activities of these hepatic enzymes, following QR or EA treatment(table 1)indicated the hepatoprotective potential of those flavonoids on the liver function (Taslidere et al 2016; Afifia et al 2016; Amin and Arbid 2017).…”

“…In the same sequence there are significant reduction in both TAC and GPX enzyme activity(Figure 1). TAA administration induced severs oxidative damage in the rat liver was reported previously byZargar et al (2017) andMiguel et al (2017). The significant reduction in the level of MDA and elevation of antioxidant status of tissue represented in significant elevation for TAC and GPX activity in liver after QR or EA treatments may be as a result of its antioxidant and free radical scavenging ability(Taslidere et al 2016; Afifia et al2016;Amin and Arbid 2017; Ansar et al 2016).…”

Protective Effect of Aqueous Extract from the Leaves of Justicia tranquebariesis against Thioacetamide-Induced Oxidative Stress and Hepatic Fibrosis in Rats

“…GST is a soluble enzyme located in the cytosol, which plays a significant function in the detoxification of xenobiotics [ 8 ]. It increases the solubility of hydrophobic substances and metabolizes toxic compounds to non-toxic ones, which means they have an increasing protective activity of the liver [ 36 ]. The increased hepatic GST activity induced by J. tranquebariensis can, therefore, reduce TAA hepatotoxicity.…”