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1.
J Environ Biol ; 2011 May; 32(3): 325-332
Article in English | IMSEAR | ID: sea-146585

ABSTRACT

Inadvertent intake of inorganic arsenic and chromium through drinking water and food causing their toxic insults is a major health problem. Intestinal bacteria including Lactobacilli play important regulatory roles on intestinal homeostasis, and their loss is known to cause gastrointestinal (GI) disorders. Probiotic Lactobacilli resistance to arsenite and chromium-VI could be an important factor for the perspective attenuation of GI-disorders caused by these toxic metals/metalloid. In the present study resistance of arsenite (up to 32 ppm), Cr-VI (up to 64 ppm), and arsenite plus Cr-VI (32 ppm each) were developed under in vitro condition following chronological chronic exposures in Lactobacilli strains. Comparative study of biochemical parameters such as membrane transport enzymes and structural constituents; dehydrogenase and esterase activity tests, which are respective indicators for respiratory and energy producing processes, and the general heterotrophic activity of cells, of resistant strains showed similarities with their respective normal parent strains. The resistant strains were also found to be sensitive to antibiotics. Findings indicate that these resistant probiotic Lactobacilli would be useful in the prophylactic interventions of arsenic and chromium GI-toxicity.

2.
J Biosci ; 1986 Mar; 10(1): 29-36
Article in English | IMSEAR | ID: sea-160587

ABSTRACT

Male albino rats were given intraperitoneal injections of choline chloride (0·1,0·33 or 0·5 × lethal dose 50) for a total period of one month and then killed at the end of 30,90 and 240 days for the study of pathotoxicokinetics of choline. Chronic choline administration in rats caused a decrease in growth rate, a dose dependent modulating effect on the somatic tissue indices of lung and lymph nodes, as well as cellularity of lymph nodes. In another experiment, the effect of choline on mica induced pulmonary lesions was studied. The combined effect of choline and mica caused adenocarcinoma of bronchiolar epithelium and marked lymphadenopathy with abnormal cells in the lymph nodes at the termination of experiment (330 days). The results of the present investigation suggest that excess choline availability not only produces pulmonary pathological lesions by itself but it also further enhances the lung lesions in altered pulmonary conditions.

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