%0 Journal Article %T Effects of sub-chronic, low-dose cadmium exposure on kidney damage and potential mechanisms %A Liu, Qiling %A Zhang, Rongqiang %A Wang, Xiang %A Shen, Xiangli %A Wang, Peili %A Sun, Na %A Li, Xiangwen %A Li, Xinhui %A Hai, Chunxu %J Annals of Translational Medicine %D 2019 %B 2019 %9 %! Effects of sub-chronic, low-dose cadmium exposure on kidney damage and potential mechanisms %K %X Background: The present study was to investigate the potential mechanisms underlying the sub-chronic low-dose cadmium (Cd) exposure induced renal injury in rats. Methods: Totally 40 male adult SD rats were randomly divided into four groups: control group, low-dose Cd group (1 mg/kg CdCl 2 ), moderate-dose Cd group (2.5 mg/kg) and high-dose Cd group (5 mg/kg). Results: From the 3 rd week, the body weight of rats in moderate-dose and high-dose declined significantly as compared to the control group (P<0.05); the liver to body weight ratio increased, the volumes of 24-hour urine and drinking-water decreased markedly (P<0.05), the BUN, SCr and β 2 -MG increased significantly, but the Fe 2+ concentration decreased markedly as compared to the control group (P<0.05); the serum MDA and SOD 1 content contents increased, but the serum SOD 2 and CAT contents decreased significantly in Cd-treated groups (P<0.05); Renal injury deteriorated with the increase in Cd dose; swelling glomeruli showed stenotic renal-tubules, and epithelial-cell-necrosis, shedding and accumulation in the lumen, massive infiltrated inflammatory cells and interstitial hyperaemia were observed; The mitochondria in renal-tubular-epithelial-cells displayed swelling, deformation and vacuolation; the renal ROS content increased in Cd-exposure-groups; the renal SOD 1 expression increased but the expression of SOD 2 and CAT decreased (P<0.05). The Bcl-2 expression decreased, but Bax expression and Bax/Bcl-2 ratio increased significantly in a Cd-dose dependent manner. Conclusions: Cd may cause renal injury in a dose dependent manner, which may be ascribed to the disordered Fe 2+ absorption, redox imbalance and apoptosis in the kidney. %U https://atm.amegroups.org/article/view/25048 %V 7 %N 8 %P 177 %@ 2305-5847