Vitamin E prevents buthionine sulfoximine-induced biochemical disorders in the rat

Abstract

Antioxidant therapy can improve the protection and metabolic activity of cells and tissues. In this study, the effect of vitamin E administration on buthionine sulfoximine (BSO)-induced glutathione (GSH) depletion in the rat lung and liver was investigated. Hepatic GSH was depleted by intraperitoneal administration of BSO (4 mmol kg(-1)), twice a day, for 30 days to rats. We also investigated whether the lung and liver mitochondrial GSH contents were influenced by BSO administration and whether an extracellular supply of vitamin E could prevent the changes caused by BSO-mediated GSH depletion. Glutathione levels in lung and liver tissues were depleted by 47% and 60%, respectively. Depletion of hepatic and pulmonary GSH in turn causes decline in the levels of mitochondrial GSH, leading to impaired antioxidant defence function of mitochondria. Both the cytosolic and mitochondrial glutathione disulfides (GSSG) were altered during BSO treatment, and led to drastic increase in GSSG/GSH redox status. One of the experimental groups was given vitamin E (65 mg (kg diet)(-1)) mixed with rat feed. The rats fed with vitamin E were found to have partially restored GSH levels in liver and lung, diminished levels of TBARS and minimized tissue damage. The current findings suggest that the impaired glutathione and glutathione-dependent enzyme status may be correlated with the elevated lipid peroxidation and mitochondrial membrane damage and that vitamin E therapy to the BSO-administered rats prevents the above changes. However, vitamin E did not have any effect on the activity of gamma-glutamyl cysteine synthetase (gamma-GCS).

The synergy of β amyloid 1-42 and oxidative stress in the development of Alzheimer’s disease-like neurodegeneration of hippocampal cells

“…We analyzed the prooxidant activity of the studied analytes and found an increase in lipid peroxidation in the BSO-treated groups (high TBARS level) and oxidative damage to proteins in the Aβ-treated groups (high levels of protein carbonylation and AOPP). These findings support in the immunocytochemistry results, indicating that the membrane was likely damaged or lost in the BSO-treated groups, and are consistent with the literature 39 .…”

l‐Buthionine (S,R) Sulfoximine Depletes Hepatic Glutathione But Protects Against Ethanol‐Induced Liver Injury

“…In vivo studies have shown that administration of BSO in the drinking water of rats causes a 4-fold increase of DNA-hydroxynoneal adducts, an elevated GSSG/GSH ratio and enhanced lipid peroxidation (Chung et al, 2005). This increase can be attenuated by administration of vitamin E (Rajasekaran et al, 2004(Rajasekaran et al, , 2005. Mice fed 20 mM BSO in the drinking water, exhibit a 54% depletion of glutathione in liver with no signs of toxicity, but coadministration of BSO with acetaminophen results in death after only 2 days of acetaminophen treatment.…”

The pharmacological potential ofSorbus commixtacortex on blood alcohol concentration and hepatic lipid peroxidation in acute alcohol-treated rats

“…ROS, such as superoxide anions, hydrogen peroxide, hydroxyl radicals and lipid peroxides, can contribute to a variety of human diseases (Yokozawa et al 2004;Badenhorst et al 2005;Maharaj et al 2005;Rajasekaran et al 2005;Zhang et al 2005) or are present in toxic conditions such as acute alcohol ingestion (Ashak et al 1991;Fernandez-Checa et al 1993;Halliwell 1997). In normal conditions, ROS are efficiently scavenged by the cellular antioxidant defence system, which includes enzymes such as SOD, catalase, glutathione peroxidase and glutathione reductase, and non-enzymatic antioxidants such as GSH and vitamins A, C, and E (Rajasekaran et al 2004;Jahangir et al 2005;Sood et al 2005). However, when the ROS produced in the tissues exceed the ability of the antioxidant system to eliminate them, oxidative stress results (Jenkins & Goldfarb 1993).…”