The Combination of Tamarindus indica and Coenzyme Q10 can be a Potential Therapy Preference to Attenuate Cadmium-Induced Hepatorenal Injury.

Cadmium (Cd) is a hazardous environmental pollutant that menaces human and animal health and induces serious adverse effects in various organs, particularly the liver and kidneys. Thus, the current study was designed to look into the possible mechanisms behind the ameliorative activities of Tamarindus indica (TM) and coenzyme Q10 (CoQ) combined therapy toward Cd-inflicted tissue injury. Male Wistar rats were categorized into seven groups: Control (received saline only); TM (50 mg/kg); CoQ (40 mg/kg); Cd (2 mg/kg); (Cd + TM); (Cd + CoQ); and (Cd + TM + CoQ). All the treatments were employed once daily via oral gavage for 28 consecutive days. The results revealed that Cd exposure considerably induced liver and kidney damage, evidenced by enhancement of liver and kidney function tests. In addition, Cd intoxication could provoke oxidative stress evidenced by markedly decreased glutathione (GSH) content and catalase (CAT) activity alongside a substantial increase in malondialdehyde (MDA) concentrations in the hepatic and renal tissues. Besides, disrupted protein and lipid metabolism were noticed. Unambiguously, TM or CoQ supplementation alleviated Cd-induced hepatorenal damage, which is most likely attributed to their antioxidant and anti-inflammatory contents. Interestingly, when TM and CoQ were given in combination, a better restoration of Cd-induced liver and kidney damage was noticed than was during their individual treatments.

Thermal stress accelerates mercury chloride toxicity in Oreochromis niloticus via up-regulation of mercury bioaccumulation and HSP70 mRNA expression.

Mercury (Hg) is an environmental pollutant that threatens aquatic life. Many environmental factors, including water temperature, are reported to influence the toxicity of dissolved chemicals in the aquatic ecosystem. Therefore, we investigated the impact of thermal stress on Hg-induced subchronic toxicity in Nile tilapia (Oreochromis niloticus). Fish were randomly allocated into five groups. Group I served as the control and kept at 25 °C. Groups II, III, IV, and V were reared at 25, 28, 31, and 34 °C, respectively, and co-exposed to HgCl2 (1/10 LC50) for 42 days. Blood and tissue samples were collected after 21 and 42 days. All HgCl2-exposed groups exhibited significant elevations in serum levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), urea, and creatinine, along with decreases in the serum total protein and albumin. In addition, marked reductions in antioxidant enzymes, including superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSPx), were observed. Remarkable increases in Hg tissue concentrations were detected along with increases in heat shock protein (HSP) 70 mRNA expression. Interestingly, the patterns data that were recorded were more coincident with the water temperature than the period of exposure. In conclusion, water temperature and exposure period are two crucial factors modulating HgCl2-induced toxicity and bioaccumulation in Nile tilapia. Our findings provide new insights concerning the impact of thermal stress as an environmental factor on Hg toxicity and bioaccumulation in Nile tilapia and, in turn, on fish and fish consumer health.