Vitamin C as a potential ameliorating agent against hepatotoxicity among alcoholic abusers.

OBJECTIVE: Drug and substance abuse remains a major medical problem globally. Alcohol consumption, particularly heavy drinking, is an important risk factor for many health problems and is a major contributor to the global burden of disease. Vitamin C has proven to be defensive against toxic substances and provides antioxidant and cytoprotective activity to hepatocytes. The aim of this study was to investigate vitamin C as a potential ameliorating agent against hepatotoxicity among alcohol abusers. PATIENTS AND METHODS: This study was a cross-sectional study that included eighty male hospitalized alcohol abusers and twenty healthy people as a control group. Alcohol abusers received standard treatment plus vitamin C. Total protein, albumin, total Bilirubin, aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), thiobarbituric acid reactive substances (TBARS), reduced glutathione (GSH), superoxide dismutase (SOD), catalase (CAT) and 8-hydroxhguanosine (8-OHdG) were investigated. RESULTS: This study reported that, in the alcohol abuser group, there was a significant increase in the total protein, bilirubin, AST, ALT, ALP, TBARS, SOD and 8-OHdG; on the other hand, there was a significant decrease in albumin, GSH and CAT compared with the control group. The alcohol abuser group treated with vitamin C showed a significant decrease in total protein, bilirubin, AST, ALT, ALP, TBARS, SOD and 8-OHdG; on the other hand, there was a significant increase in albumin, GSH and CAT compared with the control group. CONCLUSIONS: This study's findings suggest that alcohol abuse induces significant alterations in various hepatic biochemical parameters and oxidative stress and that vitamin C has a partial protective role in countering alcohol abuse-induced hepatotoxicity. Using vitamin C as an adjunctive supplement to standard treatment may be helpful in minimizing the toxic side effects of alcohol abuse.

Activation of the molecular and functional effects of Nrf2 against chronic iron oxide nanorod overload-induced cardiotoxicity.

Reactive oxygen species have a significant role in the pathogenesis of iron oxide nanorod (IONR) overload-induced organ toxicity in some organs such as the lungs. Green tea induces upregulation of phase II antioxidant enzymes that are transcriptionally organized by the nuclear factor (erythroid-derived 2)-like 2 (Nrf2) that when activated antagonize the oxidative stress induced by IONR overload that causes cardiotoxicity. The aim of the present study was to determine whether treatment of cardiotoxicity with iron chelators (deferiprone (DFP) or deferoxamine (DFO)) alone or in combination with phytochemical activation of Nrf2 (green tea) can protect cardiomyocytes from IONR overload-induced cardiotoxicity. One hundred five rats were distributed into seven groups: two control groups (non-IONR-overloaded and IONR-overloaded) and five IONR-overloaded groups such as a green tea group, DFP group, DFP combined with green tea group, DFO group, and DFO combined with green tea. Blood samples and cardiac tissues were obtained for estimation of total iron-binding capacity, ratio of myocardial 8-hydroxy-2'-deoxyguanosine/myocardial 2-deoxyguanosine, thiobarbituric acid reactive substances, glutathione (GSH) contents, and histopathological examination. The results showed mild histopathological changes in the heart and a significant decrease in all biochemical parameters, except for myocardial GSH, in the DFP group. The addition of green tea improved the biochemical and histopathological results compared with chelators alone.