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Purpose: In the present study, we aimed to identify the effect of three increasing doses of most widely preservative, formaldehyde (FA) on the urinary system using human embryonic kidney cells (HEK-293) in vitro. Materials and methods: The HEK-293 cells were grown in Dulbecco’s Modified Eagle medium (DMEM, Gibco, USA) supplemented with 10% of fetal bovine serum, 100 IU/ml penicillin and 100 μg/ml of streptomycin (Gibco, USA) using 25cm2 flasks (Nunc, Denmark), in a CO2 incubator (Heal Force) at 37°C are treated with 19 % formaldehyde in DMEM supplemented with 10% of fetal bovine serum to yield final concentrations of 0.05 μl/ml, 0.1 μl/ml, 0.5 μl/ml and 1.0 μl/mlof 19% FA. Results: The result showed that statistically significant dose dependent decrease in cell viability of HEK-293 cells with exposure to increasing concentration of FA (0.05 μl/ml, 0.1 μl/ml, 0.5 μl/ml and 1.0 μl/ml) on MTT assay. Extremely huge dose dependent DNA damage with a dose dependent up regulation of mRNA expression of pro-apoptotic iNOS and TNF- gene was observed when HEK-293 cells are treated with the increasing concentration of FA. In addition, the protein expression levels of Bcl-2 and Bax revealed that increasing concentration of FA on HEK-293 cells down regulated the anti-apoptotic Bcl-2 and up regulated pro-apoptotic Bax gene. Conclusions: Our result indicates that, high dose of FA is more dangerous than the low dose on HEK-293 cells with cellular damage.
EN
Purpose: To investigate the involvement of oxidative stress in Cadmium (Cd) induced alteration in the functional status of the liver. And to assess the efficacy of folic acid and vitamin B12 in preventing Cd-induced damage in the same. Materials and methods: The experiment was carried out for four weeks. For the experiment, 25 healthy male adult Wistar albino rats were randomly selected and were divided into five equal groups and treated as control, treated with Cd, supplemented with vitamin B12 and folic acid and in the combination of these two. After 28 days the liver function enzymes and oxidative stress parameters were measured. Results: Cd is the silent killer of the hepatic system through the induction of oxidative stress in male rats. From this investigation, it is evident that the folic acid+vitamin B12 possess significant hepatoprotective and antioxidant activity against Cd-induced hepatotoxicity in the rat model. In addition, results revealed that the folic acid alone and or in combination with vitamin B12 blunted the hepatotoxic effect significantly. Conclusions: Based on results obtained, it can be concluded that folic acid and vitamin B12 offer a protective effect in Cd-induced oxidative stress associated with hepatocellular injury. Folic acid and vitamin B12 can be considered as a potent natural antioxidant which has the capacity to provide protection against Cd-induced oxidative stress in the liver in rats. However, to elucidate the exact mechanism of this modulatory effect and to examine its potential therapeutic effects further studies are essential.
EN
Purpose: Despite people suffering from several forms of ill health, constant exposure to toxic wastes and chronic diseases as a result of mining, there is a tragic gap in the availability of ‘scientific’ studies and data on the health hazards of mining in India. This study was proposed to understand better the relationship between occupational exposure to coal, blood lipid profiles and red blood cell (RBC) functional status of coal workers. Materials and methods: Blood samples were obtained from coal miners (n=32) of an underground mine in West Bengal. Blood lipid profiles and RBC functional status were determined. Students’ t-test and Pearson correlation analyses were completed to analyze the data. Results: Compared to the control subjects, significantly higher levels of cholesterol (p<0.01), triglycerides (p<0.01), LDL (p<0.001), and VLDL (p<0.001) were observed in coal miners. HDL, Hb, Na+-K+ATPase and SOD activity were significantly (p<0.001) lower in coal miners, whereas MDA levels (p<0.001) and osmotic fragility in coal miners were increased significantly (p<0.01). Conclusions: Our study indicates that elevated MDA and antioxidant insufficiency caused disruption in the structural integrity of erythrocyte, which may be a pathophysiological mechanism in the progression of disease in coal miners. Also, cardiovascular disease risk factors were more prevalent in the coal miners.
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