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.

Green synthesis of silver nanoparticles reduced with Trigonella foenum-graecum and their effect on tumor necrosis factor-α in MCF7 cells.

OBJECTIVE: Silver nanoparticles (AgNPs) are known to exhibit anti-inflammatory and anticancer activities. They have been reported to reduce the levels of tumor necrosis factor (TNF) - a proinflammatory cytokine involved in cell proliferation, differentiation, and apoptosis - in cell lines. As patients with breast cancer have been reported to have higher serum TNF levels, we aimed at developing a novel treatment for breast cancer by evaluating the effect of Trigonella foenum-graecum extract (TFG)-reduced AgNPs on the MCF-7 cell line, which serves as a model of human breast cancer. MATERIALS AND METHODS: TFG-capped AgNPs were synthesized using a green reduction method, in which TFG reduced silver nitrate to generate AgNPs-TFG. The particle size, surface charge, ultraviolet (UV)-visible (VIS) spectra, surface morphology, % yield, and in vitro Ag+ release of the formulated AgNPs-TFG were evaluated. Additionally, the prepared NPs were examined for cytotoxicity using real-time polymerase chain reaction (real-time PCR), 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, and enzyme-linked immunosorbent assay (ELISA). RESULTS: The prepared AgNPs-TFG were uniform, small, discrete, and non-aggregated with a particle size of 22.5±0.75 nm and ζ-potential of -47.45±0.666 mV. The yield of AgNPs-TFG was 224.545±3.9 µM. Furthermore, the AgNP-TFG thin film exhibited a prolonged release of Ag+ in phosphate buffer for up to 11 h. AgNPs-TFG suppressed TNF-α expression at mRNA and protein levels in MCF-7 cells. Additionally, the formulated AgNPs-TFG did not exhibit any toxicity toward MCF-7 cells. CONCLUSIONS: This study showed that AgNP-TFG could effectively inhibit TNF-α. These results provide significant insights for developing new therapeutic strategies for cancer and other inflammatory illnesses.