This experiment was designed to investigate the extent of peroxidative changes and histological alterations in the myocardium of rats exposed to high fluoride for two generations, in addition to ameliorative role of selenium and vitamin E on the above indices. Adult albino Wistar rats were given fluoride through drinking water (200 ppm F) and maintained subsequently for two generations, while they were exposed to fluoride throughout the experiment. Fluoride treatment significantly increased the lipid peroxidation and decreased the activity of antioxidant enzymes, viz., catalase, superoxide dismutase, and glutathione level in auricle and ventricle regions of the heart. Decreased feed and water consumption, organ somatic index and marginal drop in body growth rate were observed. Decreased antioxidant enzymes and increased malondialdehyde levels might be related to oxidative damage that occurs variably in the myocardium of rats. Biochemical changes were supported by the histological observations, which also revealed that chronic exposure to fluoride causes damage to the myocardium. Results of this study can be taken as an index of cardio-toxicity in rats exposed to water fluoridation. Further, oral supplementation of selenium and vitamin E not only inhibited oxidative stress but also enhanced the activities of antioxidant enzymes. Administration of antioxidants during fluoride exposure significantly overcame cardiac fluoride toxicity and therefore may be a therapeutic strategy for fluorotic victims.
Objectives:Oxidative stress is considered as a possible molecular mechanism involved in lead (Pb2+) neurotoxicity. Very few studies have been investigated on the occurrence of oxidative stress in developing animals due to Pb2+ exposure. Considering the vulnerability of the developing brain to Pb2+, this study was carried out to investigate the effects of Pb2+ exposure in brain regions especially on antioxidant enzyme activities along with ameliorative effects of ethylenediaminetetraacetic acid (EDTA) and clinoptilolite.Methods:Three-week old developing Swiss mice Mus musculus were intraperitoneally administered with Pb2+ acetate in water (w/v) (100 mg/kg body weight/day) for 21 days and control group was given distilled water. Further Pb2+-toxicated mice were made into two subgroups and separately supplemented with EDTA and clinoptilolite (100 mg/kg body weight) for 2 weeks.Results:In Pb2+-exposed mice, in addition to increased lipid peroxidation, the activity levels of catalase, superoxide dismutase (SOD), glutathione peroxidase (GPx), and glutathione (GSH) found to decrease in all regions of brain indicating, existence of severe oxidative stress due to decreased antioxidant function. Treatment of Pb2+-exposed mice with EDTA and clinoptilolite lowered the lipid peroxidation (LPO) levels revealing their antioxidant potential to prevent oxidative stress. Similarly their administration led to recover the level of catalase, SOD, and GPx enzymes affected during Pb2+ toxicity in different regions of brain.Conclusions:The protection of brain tissue against Pb2+-induced toxicity by clinoptilolite and EDTA in the present experiment might be due to their ability to react faster with peroxyl radicals there by reducing the severity of biochemical variable indicative of oxidative damage. Thus, the results of present study indicate the neuroprotective potential of clinoptilolite and EDTA against Pb2+ toxicity.
The adverse effects produced by chlorpyrifos (CPF) or cold stress alone in humans and animals are well documented, but there is no information available relating to the consequences of their co- exposure in an age-related manner. In this study, effects of sublethal doses of CPF were carried out in vivo, for 48 h to assess the biochemical perturbations in relation to interactions with cold stress (15°C and 20°C) in different age group rat CNS. A positive interaction of CPF with age of animal and cold exposure was observed resulting in marked decrease in the activity levels of AChE (P<0.05), ChAT (P<0.05), Na+, K+-ATPase (P<0.05), Ca2+-ATPase (P<0.05), and Mg2+-ATPase (P<0.05). The ANOVA and posthoc analysis showed that regulatory enzymes decreased significantly (P<0.05) on CPF exposure. Overall, the effect of co-exposure was appreciably different from either of the exposures. Synergistic interaction of CPF and cold stress at 15°C showed higher inhibition in comparison with CPF and cold stress alone and together at 20°C. Further, this study reveals that young animals are significantly vulnerable and sensitive than adults.
Despite the enormous research in the field of Diabetology, its prevalence and complications are raising. Studies made on diabetic subjects showed deficits in cognition and memory in children suffering from long term diabetes. The relationship between cognitive dysfunction and type-1 diabetes of early onset has not been addressed properly. Hence, this study was made to investigate the effect of different duration diabetes onset on cognitive dysfunction. Using alloxan (200 mg/kg bw) induced diabetic rats learning and memory assessments were made, in addition oxidative stress indices studied. The results indicate that the duration of diabetes has significant contribution in learning and memory deficits, which were irreversible and the activity levels of CAT (P < 0.05), SOD, GST (P < 0.05), and GPx (P < 0.05) showed greater impact of free radical damage on hippocampal circuitry. The atrophic changes observed in hippocampal region corroborates the difficulties in learning and memory, and the degenerative changes were most striking in the cells of CA-1 and CA-3 hippocampal regions which could be linked to deficits in certain cognitive domains, such as memory, information processing speed, executive function, attention and motor speed. It is evident from data that brain tissue is not spared by diabetes and diabetic encephalopathy occurs due to metabolic perturbations by hyperglycaemia, insulin deficiency. The findings of this study strongly advocate that learning ability and memory have a direct relation to the duration of the diabetes. The clinical implication of the study highlights the importance of early diagnosis and treatment of juvenile diabetes induced cognitive deficits among children.
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