Treating chronic arsenic toxicity with high selenium lentil diets.

Arsenic (As) toxicity causes serious health problems in humans, especially in the Indo-Gangetic plains and mountainous areas of China. Selenium (Se), an essential micronutrient is a potential mitigator of As toxicity due to its antioxidant and antagonistic properties. Selenium is seriously deficient in soils world-wide but is present at high, yet non-toxic levels in the great plains of North America. We evaluate the potential of dietary Se in counteracting chronic As toxicity in rats through serum biochemistry, blood glutathione levels, immunotoxicity (antibody response), liver peroxidative stress, thyroid response and As levels in tissues and excreta. To achieve this, we compare diets based on high-Se Saskatchewan (SK) lentils versus low-Se lentils from United States. Rats drank control (0ppm As) or As (40ppm As) water while consuming SK lentils (0.3ppm Se) or northwestern USA lentils (<0.01ppm Se) diets for 14weeks. Rats on high Se diets had higher glutathione levels regardless of As exposure, recovered antibody responses in As-exposed group, higher fecal and urinary As excretion and lower renal As residues. Selenium deficiency caused greater hepatic peroxidative damage in the As exposed animals. Thyroid hormones, triiodothyronine (T3) and thyroxine (T4), were not different. After 14weeks of As exposure, health indicators in rats improved in response to the high Se lentil diets. Our results indicate that high Se lentils have a potential to mitigate As toxicity in laboratory mammals, which we hope will translate into benefits for As exposed humans.

Dietary intervention with iron and black tea infusion in reducing cytotoxicity of arsenic.

The relative efficacy of infusion of black tea leaf, Camellia sinensis (Linn.) O. Kuntze, (Theaceae), and iron as freshly prepared aqueous solution of ferrous sulphate in reducing the cytotoxic effects of arsenic, was tested in bone marrow cells of laboratory bred Swiss albino mice. Ferrous sulphate and tea given alone did not induce chromosomal breakage to any appreciable extent. Tea decreased chromosome damage induced by arsenic to a significant extent, while the addition of ferrous sulphate did not alter the protective action of tea against arsenic. Such protection against arsenic cytotoxicity by prolonged dietary administration of black tea infusion--a common routine beverage--is of importance in view of widespread exposure of human populations to arsenic damage through drinking water from tubewells in Eastern India and Bangladesh.

Dietary protection by iron against clastogenic effects of short-term exposure to arsenic in mice in vivo.

Iron, as freshly prepared aqueous solution of ferrous sulfate, was administered by gavage to laboratory bred Swiss albino mice. The concentration used was 152 mg/kg body weight (1/10 of the LD(50)). While screening for protection against arsenic, in one set of experiment exposure to iron was followed after 2 hr by gavaging with 2.5 mg/kg body weight (1/10 of the LD(50)) of arsenic as sodium (III) meta arsenite in distilled water. In another set, equal amounts (1:1) of ferrous sulfate and sodium arsenite were administered simultaneously. Control sets were given sodium m-arsenite alone and distilled water (vehicle). After exposure for 24 hr in all experiments, mice were sacrificed and chromosome preparations were made from bone marrow according to a colchicine-hypotonic-fixation-air-drying-Giemsa schedule. Cytogenetic endpoints screened were chromosome aberrations and divisional frequencies. Sodium arsenite alone was highly clastogenic. Ferrous sulfate, whether given together with or before exposure to sodium arsenite, reduced the clastogenic effects of the latter to a significant extent.