Fucoidan supplementation modulates hepato-renal oxidative stress and DNA damage induced by aflatoxin B1 intoxication in rats.

Aflatoxins are a common food contaminant of global concern. Aflatoxin B1 (AFB1) intoxication is associated with serious health hazards. Recently, fucoidan (FUC) has gained much attention from pharmaceutical industry due to its promising therapeutic effects. The impacts of FUC on AFB1-induced liver and kidney injures have not been sufficiently addressed. This research was conducted to evaluate the ameliorative effect of FUC in AFB1-induced hepatorenal toxicity model in rats over 14 days. Five groups were assigned; control, FUC (200 mg/kg/day, orally), AFB1 (50 µg/kg, i.p.), and AFB1 plus a low or high dose of FUC. AFB1 induced marked hepatorenal injury elucidated by substantial alterations in biochemical tests and histological pictures. The oxidative distress instigated by AFB1 enhanced production of malondialdehyde (MDA) and nitric oxide (NO) along with reduction in the reduced-glutathione (GSH), glutathione peroxidase (GSH-Px), superoxide dismutase (SOD), and catalase (CAT) activities. DNA damage in the liver and kidney tissues has been demonstrated by overexpression of proliferating cell nuclear antigen (PCNA). Unambiguously, FUC consumption alleviates the AFB1-induced mitochondrial dysfunction, oxidative harm, and apoptosis. These ameliorated effects are proposed to be attributed to fucoidan's antioxidant and anti-apoptotic activities. Our results recommend FUC supplementation to food because it exerts both preventive and therapeutic effects against AFB1-induced toxicity.

Protective potency of ascorbic acid supplementation against cytotoxicity and DNA fragmentation induced by triphenyltin on human liver carcinoma cells.

Agrochemicals are one the most significant sources of environmental pollution. Cytotoxicity and genotoxicity are the serious side effects of fungicide. In the current study, I have evaluated acute cytotoxicity and genotoxicity of triphenyltin (TPT) on human hepatic carcinoma (HepG2) cells and the ameliorating effect of ascorbic acid for 24 h. In this experiment, I have exposed HepG2 cells to ascorbic acids (50, 100, and 200 µM) simultaneously and 24 h prior triphenyltin (TPT, 400 ng/ml) exposure for 24 h to determine the protective effect of ascorbic acid by using MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) and NRU (neutral red uptake) assays. Oxidative stress, such as intracellular reactive oxygen species and glutathione levels, was measured in HepG2 cells. The intracellular reactive oxygen species was evaluated using fluorescent probe DCFDA (6-carboxy-2',7' dichloro-dihydrofluorescein diacetate). Apoptosis and genotoxicity effects of TPT in HepG2 cells were determined using flow cytometry and comet assay. The result of these experiments showed that the TPT compound (400 ng/ml) induced cytotoxicity, oxidative stress and apoptosis, and DNA damage in HepG2 cells.Ascorbic acid reduced cytotoxicity, oxidative stress, apoptosis, and genotoxicity induced by TPT. Thus, ascorbic acid is a potent antioxidant, and it showed a significant protective effect against toxicity induced by TPT in HepG2 cells.

Potential use of chromium to combat thermal stress in animals: A review.

Heat stress (HS) has adverse effects on the body: it decreases body weight, feed efficiency, feed intake, carcass quality, and nutrient digestibility. Chromium (Cr) can prevent lipid peroxidation induced by HS through its strong antioxidant activities, especially when it is added to the poultry diet. It improves the action of insulin and nutrient metabolism (of lipids, proteins, nucleic acid, and carbohydrates) through activation of enzymes associated with such pathways. The results of the studies on Cr added to diets with concentrations of 0.05 mg Cr/kg of Cr-methionine led to improved feed efficiency and DM intake by cows and Holstein dairy calves exposed to high environmental temperatures. Moreover, calves that received Cr at levels of 0.05 mg/kg of body weight tended to have higher serum concentrations of glucose and higher ratios of insulin to glucose. In heat-stressed pigs, Cr addition (200 ppb) increased blood neutrophils by about 37%. Several studies have asserted that Cr can inhibit inflammation in lactating cows by promoting the release of Hsp72, assisting production of IL-10 and inhibiting degradation of IκBα in HS conditions. In addition, Cr supplementation was observed to possibly have positive impacts on both cell-mediated and humeral immunity in heat-stressed buffalo calves. Studies over the last two decades have shown with certainty that chromium supplementation has an impact on many variables in chickens. Moreover, Cr is believed to increase insulin action in insulin-sensitive tissues (i.e., adipose and muscles), resulting in increased farm animal productivity through the improvement of feed intake, growth rate, carcass quality, reproductive parameters and immune functions.