Food Chem. Toxicol, 2014, Volume 68; Pages 99 - 107

Protective effect of dietary flaxseed oil on arsenic-induced nephrotoxicity and oxidative damage in rat kidney

Rizwan, S. Naqshbandi, A. Farooqui, Z. Khan, A.A. Khan, F

Key Findings

Exposure to uranium, lead, arsenic (As) and cadmium is common for humans in occupational and environmental settings. Metal induced toxicity involves reactive oxygen species (ROS) generation. Flaxseed oil was assessed for its ability to alleviate sodium arsenate (NaAs) nephropathy and adverse effects on kidney. NaAs treated rats fed flaxseed oil did not experience a decline in sulfhydryl groups (SHs) which are antioxidants as did controls. The authors attributed to this to arsenic being chelated to the hydroxyl groups of lignans. This is inaccurate as FXO does not contain lignans. Other mechanisms need to be determined as to how flaxseed oil is able to enhance the antioxidant capacity and to reduce free radical mediated arsenic toxicity.

ABSTRACT

Arsenic, a naturally occurring metalloid, is capable of causing acute renal failure as well as chronic renal insufficiency. Arsenic is known to exert its toxicity through oxidative stress by generating reactive oxygen species (ROS). Flaxseed, richest plant based dietary source of n 3 polyunsaturated fatty acids (PUFAs) and lignans have shown numerous health benefits. Present study investigates the protective effect of flaxseed oil (FXO) on sodium arsenate (NaAs) induced renal damage. Rats prefed with experimental diets (Normal or FXO diet) for 14 days, were administered NaAs (20 mg per kg body weight i.p.) once daily for 4 days while still on the experimental diets. NaAs nephrotoxicity was characterized by increased serum creatinine and blood urea nitrogen. Administration of NaAs led to a significant decline in the specific activities of brush border membrane (BBM) enzymes both in kidney tissue homogenates and in the isolated membrane vesicles. Lipid peroxidation and total sulfhydryl groups were altered upon NaAs treatment, indicating the generation of oxidative stress. NaAs also decreased the activities of metabolic enzymes and antioxidant defence system. Histopathological studies supported the biochemical findings showing extensive damage to the kidney by NaAs. In contrast, dietary supplementation of FXO prior to and along with NaAs treatment significantly attenuated the NaAs induced changes. (Authors abstract)

 

 

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