Effects of sub-chronic, low-dose cadmium exposure on kidney damage and potential mechanisms.

Ann Transl Med

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.

Published: April 2019

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), moderate-dose Cd group (2.5 mg/kg) and high-dose Cd group (5 mg/kg).

Results: From the 3 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-MG increased significantly, but the Fe concentration decreased markedly as compared to the control group (P<0.05); the serum MDA and SOD content contents increased, but the serum SOD 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 expression increased but the expression of SOD 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 absorption, redox imbalance and apoptosis in the kidney.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6526276PMC
http://dx.doi.org/10.21037/atm.2019.03.66DOI Listing

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