Qiling Liu1,2, Rongqiang Zhang2, Xiang Wang1, Xiangli Shen2, Peili Wang2, Na Sun2, Xiangwen Li2, Xinhui Li2, Chunxu Hai3. 1. Department of Toxicology, the Ministry of Education Key Lab of Hazard Assessment and Control in Special Operational Environment, Shaanxi Provincial Key Lab of Free Radical Biology and Medicine, School of Public Health, The Air Force Medical University, Xi'an 710032, China. 2. The Department of Epidemic and Health statistics, the College of Public Health for the Shaanxi University of Chinese Medicine, Xianyang 712046, China. 3. Department of Toxicology, School of Public Health, The Air Force Medical University, Shaanxi Provincial Key Lab of Free Radical Biology and Medicine, the Ministry of Education Key Lab of Hazard Assessment and Control in Special Operational Environment, Xi'an 710032, China.
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.
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.
Authors: Elena A Belyaeva; Larisa V Emelyanova; Sergey M Korotkov; Irina V Brailovskaya; Margarita V Savina Journal: Biomed Res Int Date: 2014-06-03 Impact factor: 3.411
Authors: Esam O Kamel; Wail M Gad-Elrab; Mohammed A Ahmed; Zuhair M Mohammedsaleh; Emad H M Hassanein; Fares E M Ali Journal: Biol Trace Elem Res Date: 2022-05-19 Impact factor: 3.738
Authors: Manish Mishra; Larry Nichols; Aditi A Dave; Elizabeth H Pittman; John P Cheek; Anasalea J V Caroland; Purva Lotwala; James Drummond; Christy C Bridges Journal: Int J Mol Sci Date: 2022-09-21 Impact factor: 6.208