F., G., A., R. (2007). ENVIRONMENTAL CADMIUM EXPOSURE:ADDITIONAL RISK FACTOR FOR TYPE II DIABETES. Egyptian Journal of Occupational Medicine, 31(2), 315-340. doi: 10.21608/ejom.2007.632
Gaballah F.; Rashed A.. "ENVIRONMENTAL CADMIUM EXPOSURE:ADDITIONAL RISK FACTOR FOR TYPE II DIABETES". Egyptian Journal of Occupational Medicine, 31, 2, 2007, 315-340. doi: 10.21608/ejom.2007.632
F., G., A., R. (2007). 'ENVIRONMENTAL CADMIUM EXPOSURE:ADDITIONAL RISK FACTOR FOR TYPE II DIABETES', Egyptian Journal of Occupational Medicine, 31(2), pp. 315-340. doi: 10.21608/ejom.2007.632
F., G., A., R. ENVIRONMENTAL CADMIUM EXPOSURE:ADDITIONAL RISK FACTOR FOR TYPE II DIABETES. Egyptian Journal of Occupational Medicine, 2007; 31(2): 315-340. doi: 10.21608/ejom.2007.632
ENVIRONMENTAL CADMIUM EXPOSURE:ADDITIONAL RISK FACTOR FOR TYPE II DIABETES
Department of Industrial Medicine and Occupational Diseases, Department of Biochemistry, Faculty of Medicine, Cairo University
Abstract
Objective: the contribution of environmental pollution to the overall risk for diabetes was assessed by evaluation to the role of inflammation and lipid peroxidation.Oxidative stress induced by accumulating cadmium in beta cells of pancreas was asuggested risk factor for type 2 diabetes. The antioxidant activities of glutathione peroxidase enzyme and sialic acid against reactive oxygen species were also investigated. Methods: levels of cadmium in blood (S-Cd) and urine (U-Cd) were measured using the graphite furnace atomic absorption spectrophotometer. Fasting glucose level (FBS), glutathione peroxidase enzyme (GSH-Px) and serum sialic acid were measured by enzymatic colorimetric assay. The glycosylated hemoglobin (HbA1c) was determined by high performance liquid chromatography.Results: the study was carried out on 26 patients diagnosed as type 2 diabetes for a mean duration of 4.66 ± 1.06 years, and a matched group of 31 non-diabetic subjects.Evaluating different life characteristics among the study population revealed an active role to rural versus urban residential areas and to current occupation in the development of diabetes in comparison to non-significant relation with feeding habits.The mean levels of serum (S-Cd) was 3.65 ± 1.17 μg/dl and 0.65 ± 0.42 μg/dl among type 2 diabetes and control groups, respectively, the difference was statistically highly significant, P<0.001. Similarly, highly statistically significant differences between the two groups were obtained for creatinine-corrected U-Cd, FBS and sialic acid, and sig- nificant differences for GSH-Px and HbA1c. Studying the associations between the different parameters, revealed that the main response variable was disease status and potential predictors included serum cadmium, creatinine-corrected urinary cadmium, residence and farming. Highly significant associations were detected for S-Cd and creatinine-corrected urinary Cd versus the kidney functions (urea, creatine and microalbuminuria),diabetes status (FBS and HbA1c), and the enzyme glutathione peroxidase.Similar results were obtained between S-Cd and sialic acid, which associated significantly with cadmium level in urine after correction for creatinine. The correlations studied between FBS and HbA1c versus the antioxidant GSH-Px as well as sialic acid proved highly significant with sialic acid only. No significant correlation was reported between the GSH-Px and the sialic acid. The effect of age, sex, body mass
index, duration and onset of diabetes were dealt with. Conclusion: Environmental pollution by the biotoxic cadmium metal has proved to be a risk factor contributing to the high incidence of type 2 diabetes among the general population. The acute phase reactant, sialic acid appeared to give new hopes by its scavenging role against the generated hydroxyl radicals, thus guarding against the possible development of diabetes. Additionally, estimation of salivary sialic acid may be used as a predictive non-invasive bio-marker of oxidative stress induced by the accumulation of cadmium in beta cells of pancreas.
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