Abstract:Objective To study the effects of sodium arsenite exposure on oxidative stress, liver function and glucose and lipid metabolism in rats, to explore the relationship between arsenic exposure and diabetes, and to provide evidence for the pathogenesis of arsenic. Methods Rats were exposed to sodium arsenite in drinking water to establish the arsenic exposure model, andhigh-fat diet plus streptozotocin to establish the type 2 diabetes mellitus (T2DM) model. After 16 weeks, we collected blood and tissue samples and then measured superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), malondialdehyde (MDA), alanine aminotransferase (ALT), aspartate aminotransferase (AST), fasting blood glucose (FBG), fasting insulin (FINS), total cholesterol (TC), triglyceride (TG), low density lipoprotein cholesterol (LDL-C) and high density lipoprotein cholesterol (HDL-C). Hematoxylin-eosin staining was used to observe the morphological changes of liver. Results Compared with the control group, the liver coefficients of rats in the diabetic model group and the high arsenic group increased (both P<0.05). The serum MDA, ALT, AST, FBG, FINS, TC, TG and LDL-C in the diabetic model group, the middle arsenic group and the high arsenic group increased significantly (all P<0.05), while SOD, GSH-Px and HDL-C decreased significantly (all P<0.05). Serum SOD ((283.38±21.14) U/ml) and GSH-Px ((3,168.01±186.32) U) of rats in the low arsenic group were higher than those in the diabetes model group ((247.94±38.70) U/ml, (2,393.81±281.19) U, both P<0.05). Serum MDA ((4.37±0.67) μmol/L, (6.18±1.10) μmol/L), ALT ((35.54±6.15) IU/L, (45.34±6.19) IU/L) and AST ((101.94±12.89) IU/L, (129.52±14.34) IU/L) in the low and middle arsenic groups were lower than those in the diabetic model group ((9.78±1.28) μmol/L, (59.75±6.38) IU/L (156.37±14.21) IU/L, all P<0.05). Serum TC ((1.58±0.32) mmol/L, (1.94±0.26) mmol/L), TG ((0.72±0.11) mmol/L, (0.94±0.15) mmol/L) and LDL-C ((0.79±0.07) mmol/L, (0.83±0.06) mmol/L) in the low and medium arsenic groups were lower than those in the diabetic model group ((3.38±0.87) mmol/L, (1.78±0.48) mmol/L, (1.22±0.16) mmol/L), while HDL-C ((1.29±0.15) mmol/L, (0.97±0.08) mmol/L) was higher than that in the diabetic model group ((0.79±0.04) mmol/L, P<0.05). No statistically significant differences were found in serum SOD, GSH-Px, MDA, ALT, AST, TC, TG, LDL-C and HDL-C between the high arsenic group and the diabetic model group (all P>0.05). Conclusion Arsenic exposure can induce oxidative stress injury in rats, resulting in liver function damage andglucose and lipid metabolism disorder. The changes in various indexes of rats in the high arsenic group tend toward those in the diabetic model group, suggesting that high arsenic exposure may be one of the risk factors for the occurrence anddevelopment of diabetes.
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