Alfa-Lipoic Acid Controls Tumor Growth and Modulates Hepatic Redox State in Ehrlich-Ascites-Carcinoma-Bearing Mice

The effect of oral supplementation ofα-lipoic (LA) on growth of Ehrlich ascites carcinoma cells (EACs) and hepatic antioxidant state in mice was investigated. The results revealed thatα-lipoic (LA) acid at 50 mg/kg body wt reduced the viability and volume of EAC cells and increased the survival of the treated animals. In addition, LA normalized oxidative stress in liver of mice-bearing EAC cells evidenced by increasing the levels of total thiols, glutathione, glutathione-S-transferase, superoxide dismutase, and catalyse. On the other hand, significant decreases in the levels of malondialdehyde and protein carbonyl were demonstrated in liver indicating controlled oxidative stress in these animals. As a consequence, LA regulated liver enzymes, alkaline phosphatase, aspartate aminotransferase, alanine aminotransferase, and gamma-glutamyl transferase. The data also indicated the efficiency of LA as cancer inhibitor and therapeutic influence. In conclusion, the present data suggest LA as a potential therapeutic complement in the treatment or prevention of different pathologies that may be related to an imbalance of the cellular oxidoreductive status associated with malignancy.

The effect of methylene blue on the hepatocellular redox state and liver lipid content during chronic ethanol feeding in the rat

Feeding of ethanol in a liquid diet to male Wistar rats caused decreases in the hepatic cytosolic and mitochondrial [NAD+]/[NADH] ratios. This redox-state change was attenuated after 16 days of feeding ethanol as 36% of the total energy intake. Supplementation of the ethanol-containing liquid diet with Methylene Blue largely prevented the ethanol-induced redox state changes, but did not significantly decrease the severity of the hepatic lipid accumulation that resulted from ethanol ingestion. Methylene Blue did not affect body-weight gain, ethanol intake or serum ethanol concentrations in ethanol-fed rats, nor did the compound influence the hepatic redox state or liver lipid content of appropriate pair-fed control animals. These findings suggest that the altered hepatic redox state that results from ethanol oxidation is not primarily responsible for the production of fatty liver after long-term ethanol feeding in the rat.