Original Article
Effects of sub-chronic, low-dose cadmium exposure on kidney damage and potential mechanisms
Abstract
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 CdCl2), moderate-dose Cd group (2.5 mg/kg) and high-dose Cd group (5 mg/kg).
Results: From the 3rd 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 β2-MG increased significantly, but the Fe2+ concentration decreased markedly as compared to the control group (P<0.05); the serum MDA and SOD1 content contents increased, but the serum SOD2 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 SOD1 expression increased but the expression of SOD2 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 Fe2+ absorption, redox imbalance and apoptosis in the kidney.
Methods: Totally 40 male adult SD rats were randomly divided into four groups: control group, low-dose Cd group (1 mg/kg CdCl2), moderate-dose Cd group (2.5 mg/kg) and high-dose Cd group (5 mg/kg).
Results: From the 3rd 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 β2-MG increased significantly, but the Fe2+ concentration decreased markedly as compared to the control group (P<0.05); the serum MDA and SOD1 content contents increased, but the serum SOD2 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 SOD1 expression increased but the expression of SOD2 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 Fe2+ absorption, redox imbalance and apoptosis in the kidney.
