10 research outputs found
Plasma nitric oxide (no) and tumor necrosis factor-α (tnf-α) levels, adenosine deaminase (ada), gamma glutamyl transferase (ggt) activities and to determine the rate of lymphocytes in the peripheral blood leukocytes alpha naphthyl acetate esterase (anae) in cattle with leptospirosis
The protective effects of l-carnitine against lead (ii) acetate toxicity in capoeta capoeta (guldensteadt 1773)
Histopathologic, biochemical and genotoxic investigations on chronic sodium nitrite toxicity in mice
PubMed ID: 24947405The aim of this study was to investigate the effects of long term Sodium nitrite (NaNO2) consumption. Swiss albino mice were given NaNO2 (0, 10 and 20mg/kg/day) as mixed in feed for 8 months. At the end of treatments, animals were sacrificed and selected organs were processed for histopathologic, imunohistochemical, biochemical and genotoxic investigations. Mild to moderate degenerative changes were observed in liver, kidney, intestine, lung and spleen of NaNO2-given mice. Inducible nitric oxide synthase and nitrotyrosine activities increased in liver and kidney of NaNO2-given mice. Proliferating cell nuclear antigen activity increased in liver. Apoptotic cell death was observed in livers of the treatment groups. Liver malondialdehyde level was higher in the treatment groups while no change was seen in kidney. Nitric oxide levels in both liver and kidney of the treatment groups were lower than those of the control group. In genotoxic investigations, the number of chromosome and chromatid breaks, chromatid association, and polyploidy increased while mitotic index decreased in NaNO2-given mice. The results showed that NaNO2 would cause histopathologic changes, nitrosative tissue damage, and lipid peroxidation in liver and kidney, as well as induce chromosomal aberrations even if it was given at low levels for long time. © 2014 Elsevier GmbH