Flaxseed oil ameliorates mercuric chloride-induced liver damage in rats.

BACKGROUND: Mercury is a relentless pollutant, and its toxicity contributes to significant health problems due to exposure to the environment. The present study has determined the impact of flaxseed oil on mercuric chloride (HgCl2)-mediated hepatic oxidative toxicity in rats. METHODS: Twenty-four healthy male Wistar rats were divided into four groups with six animals in each group. Group-A was the Control group treated with saline; Group-B received 1.0 ml oral dosage of flaxseed oil; Group-C was given 200 µl intraperitoneal injection of HgCl2, and Group-D received 1.0 ml oral dosage of flaxseed oil (one hour after treatment with 200 µl intraperitoneal injection of HgCl2. RESULTS: Mercuric chloride (HgCl2) increased the production of malondialdehyde (MDA), reactive oxygen species (ROS), glutathione (GSH), and the concentration of HgCl2 in the liver tissue with a simultaneous decrease in the activities of Superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px). Furthermore, serum HgCl2 elevated the activity of alanine transaminase (ALT) and Lactate dehydrogenase (LDH). Histopathological changes showed that liver injury was caused by mercuric chloride. Treatment with flaxseed oil ameliorated ROS production and reversed enzymes in serum and liver. Also, a noticeable improvement was observed in all the histopathological characteristics in the rats. CONCLUSIONS: The findings of this study concluded that flaxseed oil had an outstanding remedial effect on mercuric chloride-mediated hepatic cytotoxicity.

Evaluation of protective efficacy of flaxseed lignan-Secoisolariciresinol diglucoside against mercuric chloride-induced nephrotoxicity in rats.

The toxicity of heavy metals such as mercury (Hg) in humans and animals is well documented. The kidney is the primary deposition site of inorganic-Hg and target organ of its toxicity. The present study investigated the protective efficacy of flaxseed lignan-Secoisolariciresinol diglucoside (SDG) on nephrotoxicity induced by mercuric chloride (HgCl2). Rats were intraperitoneally injected with HgCl2 (2 mg/kg/day) and renal toxicity was induced. Subcutaneous administration of rats with SDG (5 mg/kg/day) as a pre-treatment caused a significant reversal of HgCl2 induced increase in blood urea, creatinine, glutathione s-transferase and catalase (CAT). On the other hand, administration of SDG with HgCl2 restored normal levels of albumin and superoxide dismutase (SOD). Histological examination of kidneys confirmed that pre-treatment of SDG before HgCl2 administration significantly reduced its pathological effects. Thus, the results of the present investigation suggest that SDG can significantly reduce renal damage, serum and tissue biochemical profiles caused by HgCl2 induced nephrotoxicity. Hence, SDG may be recommended for clinical trials in the treatment of kidney disorders caused by exposure to Hg.