| PrefaceCadmium is one of the main heavy metal pollutants, acute or chronic Cadmium contact can cause the body’s liver, kidney, lung, testicular and organ dysfunction.Selenium is one of the essential trace elements that in mammals exerts its most important function probably via selenium-dependent glutathione peroxidase. It has been shown that administration of Se com pounds effectively protects against Cd-induced toxicity. However, high dosage Se-induced toxicity and even lethality are not very well known. This study was conducted to elucidate the response of antioxidant defense system (AOS) in rats to chronic treatment with Cd or Cd+Se simultaneously.MethodsThe experiments were carried out with60-days-old male Sprague-Dawley albino rats weighing100±10g at the beginning of experiments. The animals were housed in individual cages at21±2℃and exposed to12hour light-dark cycle. They were allowed to feed and drink tap water ad libitum. The experimental groups of animals were supplied for2weeks,4weeks and8weeks with water containing30mg/L Cd (as CdC12),5μmol/kg body Se and10μmol/kg body weigh Cd+Se (CdC12+Na-selenite) in the whole experiment, respectively. Each experimental group consisted of eighteen animals. Rats (six from each group) from all the groups were sacrificed24h after last dose on2nd,4th and8th week after initiation of the experiment under light ether anesthesia. Animals were fasted overnight before sacrifice. Kidneys、livers and testiculars were reached with an abdominal middle-line incision and were then removed and separated from the surrounding tissues, washed with distilled water and immediately fixed in10%formaldehyde solution fixative. These fixed tissueswere dehydrated in an ethanol gradient, treated with a clearing agent, infiltrated and embedded in paraffin, sectioned at6um, floated on a heated water bath and mounted to glass slides. After drying overnight, paraffin was removed with a clearing agent, tissuewas rehydrated in an ethanol gradient and then stainedwith hematoxylin and eosin (HE) for light microscopic examination. And blood was immediately collected in tubes. Serum and red blood cells were separated by differential centrifugation (5min,2000g,4℃, Janetzki T32). Serum,kidneys and livers were used for the determination of glutathione peroxidase (GSH-Px), superoxide dismutase (SOD)and malondialdehyde(MDA).ResultsIn vivo studies, drinking chlorinated cadmium contained water (30mg/L) can cause significant nephrotoxicity toxicity in rats. Since2weeks, including the increase of the vitality of GSH-Px and SOD, the formation of MDA in serum, liver and kidney cortex were significantly higher than that of the control (P<0.05). With low doses (5u mol/kg) sodium selenite intervention rats, serum, liver tissue and the cortex glutathione peroxidase (GSH-Px)vigor and vitality in superoxide dismutase (SOD) are increased, malondialdehyde reduced. With simple group compared with cadmium, significant difference (P<0.01). Drinking water contain chlorinated cadmium (30mg/L) and add in doses (10μ mol/kg) sodium selenite intervention rats, serum, liver tissue and the cortex glutathione peroxidase vigor and vitality in superoxide dismutase (SOD) are increased, malondialdehyde reduced. With simple group compared with cadmium, significant difference (P<0.05).Pathological changes:In control rats kidney contained numerous nephrons which are the functional filtering unit. Each nephron was divisible into a dilated portion-the renal corpuscle, the proximal tubule, loops of Henle and distal tubules. The kidney of rats drinked with30ml/L of cadmium chloride exhibited no istological change up to2week.Following4week cadmium treatment, the glomeruli exhibited swelling thus there remained almost no space between the Bowman’s capsule and glomerulus. The tubular epithelium increased thus almost no lumen was visible. However,occasional dilatation of tubules, vacuolization and degeneration of tubular epithelial cells were noted. After6week cadmium exposure, shrinkage of few glomeruli was noticed thus increasing urinary space. There were many degenerating glomeruli. Pronounced dilatation and extensive degeneration occurred among tubules. In medulla, several tubules were degenerated and with deposition of eosin-positive substances after8weeks cadmium exposure.ConclusionThe data presented here demonstrate that oral intake of Cd results in accumulation of Cd in the kidneys of rats, which is accompanied enzymatic compounds of AOS.Contain chlorinated drinking water can cause kidney organization damaged. The vitality of GSH-Px and SOD were decreased, MDA content were increased.Increased over time, We can observe Shrinkage of glomerulus after cadmium (with water containing30mg/L Cd)treatment.Note the increased space between the glomerulus and Bowman’s capsule and the degeneration of tubules. Administration of Se compounds has been shown to protect effectively against the Cd-induced toxicity. Early use sodium selenite can protect liver and kidney from organization oxidatie stress damage by chlorinated cadmium. Oral intake of Se as Na-selenite, as one may expect, im proves AOS in the kidney of rats. Activity of kidney,liver GSH-Px and total SOD were increased in Se-treated rats. |
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