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[A study on apoptosis and activity of SAPK/JNK in adrenocortical cells induced by cadmium chloride].

Min Zhao, Xiaofang Yang, Quan Wei, W Chen, Cheng Jiang Lu, T Chen

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Abstract

OBJECTIVE: To study apoptosis induced by cadmium chloride and the alteration in activity of stress activated protein kinase (SAPK) in adrenocortical cells. METHODS: Fasciculata-glomerulosa (FG) cells of male guinea pigs were dispersed and primarily cultured in vitro. Features of apoptotic cells were observed using combined labeling with annexin-V and propidium iodide (PI) and flow cytometry, and activity of SAPK was determined with immunoprecipitation and chemiluminescence assay. RESULTS: Apoptosis rate of FG cells increased with dose of cadmium chloride (CdCl(2)) two hours after treatment with 6.25 - 200.00 micromol/L of it. The average percentages of apoptotic cells ranged from 9.90% to 82.35%, with significant difference in the groups treated with 25, 50, 100 and 200 micromol/L of CdCl(2), as compared with the control group (P < 0.01). Regression analysis showed that occurrence of apoptosis correlated with the dose of cadmium chloride in a dose-response pattern. In the meanwhile, there were obviously elevated percentages of apoptotic cells as the increase in duration of incubation, ranging from 5.58% to 73.08% for incubating cells with 50.00 micromol/L of CdCl(2), from 15 minutes to four hours. Duration of incubating cells with cadmium chloride correlated to occurrence of apoptosis in a time-effect manner. There were no remarkable changes in the activity of SAPK in adrenocortical cells two hours after incubation with 25.00 - 100.00 micromol/L of CdCl(2). CONCLUSIONS: Apoptosis can be induced by cadmium chloride in adrenocortical cells and its mechanism should be studied further.

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What this paper is about

OBJECTIVE: To study apoptosis induced by cadmium chloride and the alteration in activity of stress activated protein kinase (SAPK) in adrenocortical cells. METHODS: Fasciculata-glomerulosa (FG) cells of male guinea pigs were dispersed and primarily cultured in vitro. Features of apoptotic cells were observed using combined labeling with annexin-V and propidium iodide (PI) and flow cytometry, and activity of SAPK was determined with immunoprecipitation and chemiluminescence assay. RESULTS: Apoptosis rate of FG cells increased with dose of cadmium chloride (CdCl(2)) two hours after treatment with 6.25 - 200.00 micromol/L of it. The average percentages of apoptotic cells ranged from 9.90% to 82.35%, with significant difference in the groups treated with 25, 50, 100 and 200 micromol/L of CdCl(2), as compared with the control group (P < 0.01). Regression analysis showed that occurrence of apoptosis correlated with the dose of cadmium chloride in a dose-response pattern. In the meanwhile, there were obviously elevated percentages of apoptotic cells as the increase in duration of incubation, ranging from 5.58% to 73.08% for incubating cells with 50.00 micromol/L of CdCl(2), from 15 minutes to four hours. Duration of incubating cells with cadmium chloride correlated to occurrence of apoptosis in a time-effect manner. There were no remarkable changes in the activity of SAPK in adrenocortical cells two hours after incubation with 25.00 - 100.00 micromol/L of CdCl(2). CONCLUSIONS: Apoptosis can be induced by cadmium chloride in adrenocortical cells and its mechanism should be studied further.

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Available abstract

OBJECTIVE: To study apoptosis induced by cadmium chloride and the alteration in activity of stress activated protein kinase (SAPK) in adrenocortical cells. METHODS: Fasciculata-glomerulosa (FG) cells of male guinea pigs were dispersed and primarily cultured in vitro. Features of apoptotic cells were observed using combined labeling with annexin-V and propidium iodide (PI) and flow cytometry, and activity of SAPK was determined with immunoprecipitation and chemiluminescence assay. RESULTS: Apoptosis rate of FG cells increased with dose of cadmium chloride (CdCl(2)) two hours after treatment with 6.25 - 200.00 micromol/L of it. The average percentages of apoptotic cells ranged from 9.90% to 82.35%, with significant difference in the groups treated with 25, 50, 100 and 200 micromol/L of CdCl(2), as compared with the control group (P < 0.01). Regression analysis showed that occurrence of apoptosis correlated with the dose of cadmium chloride in a dose-response pattern. In the meanwhile, there were obviously elevated percentages of apoptotic cells as the increase in duration of incubation, ranging from 5.58% to 73.08% for incubating cells with 50.00 micromol/L of CdCl(2), from 15 minutes to four hours. Duration of incubating cells with cadmium chloride correlated to occurrence of apoptosis in a time-effect manner. There were no remarkable changes in the activity of SAPK in adrenocortical cells two hours after incubation with 25.00 - 100.00 micromol/L of CdCl(2). CONCLUSIONS: Apoptosis can be induced by cadmium chloride in adrenocortical cells and its mechanism should be studied further.

Key concepts: Cadmium chloride, Apoptosis, Propidium iodide, Annexin, Chemistry, Flow cytometry, Internal medicine, Endocrinology

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[A study on apoptosis and activity of SAPK/JNK in adrenocortical cells induced by cadmium chloride]. — Research Paper | ScholarLens