Ameliorative effects of nutritional minerals on lead-induced hematological alterations in male Wistar albino rats.

The deficiency of essential minerals increases lead absorption and thus aggravates the lead-induced toxic effects. This study was aimed at understanding the ameliorative effect of essential minerals on lead-induced alterations in hematological parameters in rats. To achieve this objective, the study was conducted in 320 male Wistar albino rats, grouped into two, with equal numbers. One of the groups of rats was fed on a mineral-supplemented food referred to as a 'well-nourished group' and another group 'undernourished group' on food without mineral supplements. Each group of rats was further subdivided into 'Subjects' and 'Controls.' Subjects of both the groups of rats were exposed to 500 ppm lead acetate up to a period of 300 days (10 months) in drinking water and the role of minerals on lead-induced alterations in hematological parameters was evaluated. A significant decrease (p < 0.001) in hemoglobin (Hb) and δ-aminolevulinic acid dehydratase (δ-ALAD) levels and a significant increase (p < 0.001) in urinary δ-aminolevulinic acid (δ-ALAU) levels were seen in subjects without mineral supplementation compared to those fed on a mineral-enriched diet. A positive correlation was observed between blood lead levels (PbB) and δ-ALAU (r = 0.792) and a negative correlation with Hb (r = -0.926) and δ-ALAD (r = -0.836) in the subjects. These changes were very prominent in the undernourished subjects when compared to the well-nourished subjects. Observations of the present study indicate that mineral supplementation with ongoing lead exposure may help in minimizing the absorption of lead and reduce lead-induced toxic effects.

Hepatotoxic effect of lead and hepatoprotective effect of Hydrilla verticillata on hepatic transcriptional and physiological response in edible fish Labeo rohita.

Lead tops the list of developmental toxicants released by industry into the environment according to Commission for Environmental Corporation. Hydrilla verticillata is an aquatic weed and rich source of variable nutrients and chemical constituents like saponins, vitamins, minerals, antioxidants, amino acids, detoxifying agents, etc. This weed is used in a beneficial way to detoxify lead in fish model. The fish were treated with sublethal concentration of lead to induce liver damage and fed with supplementary feed containing 20% of hydrilla dry powder. The present work revealed that lead accumulation is highly toxic to liver. Lead toxicity increased the expressions of cytochrome P450 1 A (CYP1A) and cytochrome P450 3 A (CYP3A) when compared to control. The metal binding stress proteins, heat shock proteins (Hsp60 & Hsp70) and metallothionein were also upregulated due to lead toxicity. Lead intoxicated fish exhibited reduced δ-aminolevulinic acid dehydratase activity in the blood, leading to reduced red blood cell count and changes in cell morphology. The lead toxicity also decreases the level of liver marker enzymes alanine transaminase, aspartate transaminase in serum. In hydrilla supplemented protective group, there was amelioration of these changes. Administration of supplementary feed to the lead intoxicated protective group significantly decreased the expressions of CYP1A, CYP3A, Hsp60, Hsp70 and metallothionein genes. The red blood cell count in lead intoxicated fish was maintained almost normal due to the protective action of Hydrilla verticillata in the diet. The observed increase in the enzymes, which further confirmed the protective effect of Hydrilla verticillata against lead induced toxicity.

Effectiveness of (PhSe)2 in protect against the HgCl2 toxicity.

This work investigated the preventive effect of diphenyl diselenide [(PhSe)2] on renal and hepatic toxicity biomarkers and oxidative parameters in adult mice exposed to mercury chloride (HgCl2). Selenium (Se) and mercury (Hg) determination was also carried out. Mice received a daily oral dose of (PhSe)2 (5.0mg/kg/day) or canola oil for five consecutive days. During the following five days, the animals were treated with a daily subcutaneous dose of HgCl2 (5.0mg/kg/day) or saline (0.9%). Twenty-four hours after the last HgCl2 administration, the animals were sacrificed and biological material was obtained. Concerning toxicity biomarkers, Hg exposure inhibited blood δ-aminolevulinic acid dehydratase (δ-ALA-D), serum alanine aminotransferase (ALT) activity and also increased serum creatinine levels. (PhSe)2 partially prevented blood δ-ALA-D inhibition and totally prevented the serum creatinine increase. Regarding the oxidative parameters, Hg decreased kidney TBARS levels and increased kidney non-protein thiol levels, while (PhSe)2 pre-treatment partially protected the kidney thiol levels increase. Animals exposed to HgCl2 presented Hg content accumulation in blood, kidney and liver. The (PhSe)2 pre-treatment increased Hg accumulation in kidney and decreased in blood. These results show that (PhSe)2 can be efficient in protecting against these toxic effects presented by this Hg exposure model.