ABSTRACT
Objective To study the molecular mechanism of renal injury of chronic arsenic poisoning rats induced by the expression of cysteine caspase-8 and P53 in renal proximal tubular epithelial cells.Methods Sixty healthy SD rats were divided into three groups,high-,low-dose group,and control group,n =20 in each group.The rats in high and low dose groups were treated with As203 through drinking water,10.0 and 0.4 mg/kg,respectively.The control rats were given distilled water.Four months later,serum and urinary arsenic level was determined,and kidney specimens were taken.The expression of cysteine caspase-8 and P53 in renal proximal tubular epithelial cells was detected by histological technique-HE staining and SABC immunohistochemistry.In addition,cell number counting and image analyses were used in the study.Results The number of caspase-8 positive cells of renal proximal tubule in control group,low-and high-dose group was 3.33±1.32,31.14±8.02 and 46.50±7.20 cell number/visual fields,respectively,which was increased with dose increasing(all P ＜0.05);the average gray value was 151.34±6.40,133.58±4.63 and 128.34±16.28,respectively,decreased with dose increasing(all P ＜0.05).The number of P53 positive cells was 3.17±1.59,26.29±4.23 and 47.00±6.22 cell number/visual fields,respectively,increased with dose increasing (all P ＜ 0.05) ; the average gray value was 142.54±8.06,121.48±5.68 and 101.89±6.35,respectively,decreased with dose increasing (all P ＜ 0.05).Conclusion The increase of caspase-8 and P53 positive cells is one of the molecular mechanisms of renal injury induced by arsenic poisoning.
ABSTRACT
ObjectiveTo investigate the expression and relevant function of protein kinase C (PKC)-α in kidney of rat with chronic arsenic poisoning.MethodsTotally 60 healthy SD rats of clean grade were randomly divided by body weight into 3 groups:high-dose arsenic exposure group (10.0 mg/kg),low-dose arsenic exposure group (0.4 mg/kg),and control group.The rats were exposed by drinking arsenic solution which was mixed with distilled water.Rats were weighed every 10 days and dose volume of arsenic solution was adjusted.After continuous exposure for 4 months,blood and urinary arsenic were determined.Rat kidneys were taken and stained by Immunohistochemistry SABC.PKC-o positive cells in the kidney were observed and counted,and its average gray value was analyzed with image analysis software (Biomias).ResultsProximal tubules PKC-α-positive cell count [(3.62 ± 1.90),(10.07 ± 3.22)/field],glomerular PKC-α-positive cell count [(3.62 ± 1.90),(10.07 ± 3.22)/field]in high and low arsenic group of SD rat kidney were lower than those of the control group [(60.00 ± 9.63),(18.57 ± 2.71/field,all P ＜ 0.05]; both urinary arsenic level[(7366.62 ± 1086.50),(1744.31 ± 300.12)μg,/L]and blood arsenic level [(31.59 ± 9.24),(16.58 ± 2.08)μg/L] in high-dose and low-dose groups were higher than those of the control group [(18.97 ± 3.58),(18.97 ± 3.58)μg/L,all P ＜ 0.05] ; the average gray values of SD rat kidney proximal tubule,glomerular PKC-o positive cells in high-dose and low-dose groups( 142.79 ± 11.16,122.15 ±5.91 ) were higher than that of the control group (114.33 ± 6.70,all P ＜ 0.05).ConclusionsArsenic can decrease SD rat kidney PKC-α -positive cells.The regulatory function of PKC-o in inhibiting cell apoptosis of kidney of rats with arsenic poisoning is weakened.