[Renal damage of indium sulfate on rats].

OBJECTIVE: To study the renal damage of indium sulfate. METHODS: 32 healthy Wistar rats were randomly and equally divided into 3 dose groups( 52. 3 mg/kg、104. 6 mg/kg 261. 4 mg/kg) and one negative control group. Indium sulfate were orally given once a day successively 5 days a week for 8 weeks. Each group of rats was collected24 hour urine after the end of the posion. We tested the content of Cr, BUN, T-AOC, ALB in serum and the GSH activity in kidney by kids and detected the β2-MG content in serum and urine by ELISA test. Inductively coupled plasma mass spectrometry( ICP-MS)method was used to detect the content of indium in whole blood, urine and kidney tissue of rats. Hematoxylin and eosin( H&E) staining was used to detect histological changes. RESULTS: During the experiment, all the rats were normal in activities, feed and drinking water, and they developed stably. In the period of seventh weeks and eighth weeks, the body weight of rats in high dose group was significantly lower than the control group( P <0. 05). Compared with the control group[( 1. 27 ± 0. 55), ( 0. 40 ± 0. 01) and( 0. 30 ±0. 06) μg/L], 3 dose group of indium in blood[( 44. 10 ± 23. 10), ( 52. 08 ± 21. 03) and( 67. 42 ± 45. 98) μg/L], urine[( 0. 72 ± 0. 13), ( 2. 75 ± 0. 15) and( 4. 31 ± 0. 33)μg/L]and kidney [( 1. 36 ± 0. 83), ( 1. 52 ± 0. 49) and( 2. 87 ± 0. 20) μg/L] were significantly increased( P < 0. 05). The level of Cr in serum in the high dose group were significantly higher than that in the control group [( 66. 06 ± 18. 62) and( 46. 53 ± 7. 95)μmol/L, P < 0. 05], the serum BUN content[( 3. 98 ± 0. 82) and( 4. 09 ± 0. 71) mmol/L] in the high dose group and middle dose group were significantly lower than the control group [( 4. 77 ± 0. 49) mmol/L, P < 0. 05]. Compared with the control group, 3 dose group of the β2-MG in serum and urine were significantly increased( P < 0. 05), and the level of T-AOC[( 4. 87 ± 2. 36), ( 4. 50 ± 2. 33) and( 4. 00 ± 3. 29) U/m L] in serum and GSH[( 6. 41 ± 1. 86), ( 5. 06 ± 2. 09) and( 2. 77 ± 2. 64) μmol/( g prot) ] in renal tissue were significantly decreased[( 15. 20 ± 5. 43) U/m L and( 14. 74 ± 6. 47) μmol/( g prot), P < 0. 05]. Compared with the control group, the middle and high dose exposure group had significant inflammatory pathological changes, mainly manifested as glomerular swelling, renal tubular structure abnormalities and inflammatory cell infiltration. CONCLUSION: Indium sulfate can cause the accumulation of indium in the kidney, oxidative damage, pathological changes and dysfunction in the kidney of rats.