| Cadmium is a non-essential and toxic heavy metal for human, ubiquitous in the environment. Kidney is the critical target organ for subchronic exposure to cadmium. Many scholars studied the kidney toxicity of the cadmium in rodents such as rats and mice previously. However, there are great differences between rodents and human in size and genes, so those experimental results couldn't well reflect the degree of possible injuries of cadmium to human body. In addition, many recent epidemiological studies showed that the critical concentrations of cadmium toxicity had been overestimated. This research was to study the kidney toxicity of cadmium with pigs as experimental animal, it could provide further theoretical data for prevention and monitoring of cadmium renal toxicity for their genetic relationship is closer to human.20 inbred strain pigs were randomly divided into five groups, each for four, and they were fed for 100 days with normal feeds and feeds added with the cadmium with the content of 0.5,2.0,8.0,32.0 mg/kg, respectively. The body weight was measured, the urine and blood was collected every 20 days. After continuously feeding for 100 days, the pigs were killed and their hearts, livers, spleens, lungs, kidneys, muscle, duodenums, large intestines, small intestines, stomachs, bladders, femurs, ribs, brains, cerebellas, ears, derma, tails and tongues were collected to determine the cadmium content by microwave digestion-AAS. Kidney was collected to determine its kidney index, and observe its pathological changes with pathological sections by H·E staining method. Kidney cortical was collected to determine the activity of SOD, CAT, GSH-Px and content of MDA by spectrophotometer. Uβ2-MG, Uα1-MG, UNAG, Cd-MT and URBP were measured by means of enzyme linked immunoabsorbent assay (ELISA). Threshold dose of kidney damage was calculated by benchmark dose method. The main conclusions were as follows:1) Under the conditions of subchronic cadmium exposure, cadmium in pigs mainly distributed in kidney, liver, duodenum, spleen. Kidney cortex is the most important part for cadmium accumulation;2) Cadmium exposure less than 32.0 mg/kg could not significantly inhibit the growth of Wuzhishan pigs, or cause lipid peroxidation damage. Cadmium exposure higher than 0.5 mg/kg could cause renal tubular epithelial cell swelling, and tubular stenosis. The degree of damage of kidney pathological damage aggravate with the increasment of cadmium exposure dose;3) Blood cadmium levels showed a dose-response relationship with cadmium exposure, which suggests that blood cadmium levels is effective indicator for recent cadmium exposure. Urine cadmium concentration can reflect both the cadmium exposure dose and the kidney dysfunction. Urine cadmium concentration is a reliable biomarker of cadmium exposure.4) Subchronic cadmium exposure gave rise to renal tubular dysfunction, which was reflected by low-molecular-weight proteinuria. There were good consistencies when UCd-MT, UNAG, Uβ2-MG, URBP were used as effect biomarkers of cadmium induced renal damage. The estimated BMDL were 1.00, 0.88, 3.08, 0.67 mg Cd/kg for UCd-MT, UNAG, Uβ2-MG and URBP, respectively. URBP was a sensitive effect biomarker for early renal damage.5) The threshold dose of subchronic cadmium exposure induce renal damage was 0.67 mg/kg, and when it was used as a reference point for the health guideline value derived ADI was 0.2μg/kg·BW. |
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