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Environ Toxicol Pharmacol. 2014 Nov;38(3):800-6. doi: 10.1016/j.etap.2014.09.013. Epub 2014 Sep 30.

Effect of melamine on [Ca(2+)]i and viability in PC3 human prostate cancer cells.

Author information

1
Department of Surgery, Kaohsiung Veterans General Hospital, Kaohsiung 81362, Taiwan.
2
Department of Nursing, Division of Basic Medical Sciences, Chang Gung Institute of Technology, Chia-Yi 61363, Taiwan; Chronic Diseases and Health Promotion Research Center, Chang Gung Institute of Technology, Chia-Yi 61363, Taiwan.
3
Division of Pediatrics, St. Joseph Hospital, Kaohsiung 80288, Taiwan.
4
Department of Medical Education and Research, Kaohsiung Veterans General Hospital, Kaohsiung 81362, Taiwan.
5
Department of Medicine, Kaohsiung Veterans General Hospital, Kaohsiung 81362, Taiwan.
6
Department of Rehabilitation, Kaohsiung Veterans General Hospital, Kaohsiung 81362, Taiwan.
7
Department of Dermatology, Kaohsiung Veterans General Hospital, Kaohsiung 81362, Taiwan.
8
Department of Nursing, Tzu Hui Institute of Technology, Pingtung 92641, Taiwan.
9
Department of Pharmacy, Tajen University, Pingtung 90741, Taiwan.
10
Department of Medical Education and Research, Kaohsiung Veterans General Hospital, Kaohsiung 81362, Taiwan. Electronic address: crjan@isca.vghks.gov.tw.

Abstract

Melamine is thought to be an endocrine disrupter that affects physiology in cells. This study examined the effect of melamine on cytosolic free Ca(2+) concentrations ([Ca(2+)]i) and viability in PC3 human prostate cancer cells. Melamine evoked [Ca(2+)]i rises concentration-dependently. Melamine-evoked Ca(2+) entry was inhibited by nifedipine, econazole, SKF96365, GF109203X and phorbol 12-myristate 13 acetate. In Ca(2+)-free medium, treatment with the endoplasmic reticulum Ca(2+) pump inhibitor thapsigargin inhibited melamine-evoked [Ca(2+)]i rise. Conversely, treatment with melamine abolished thapsigargin-evoked [Ca(2+)]i rise. Inhibition of phospholipase C with U73122 did not alter melamine-evoked [Ca(2+)]i rise. Melamine at 500-800μM decreased cell viability, which was not reversed by pretreatment with the Ca(2+) chelator 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid-acetoxymethyl ester (BAPTA/AM). Collectively, our data suggest that in PC3 cells, melamine induced [Ca(2+)]i rises by evoking phospholipase C-independent Ca(2+) release from the endoplasmic reticulum, and Ca(2+) entry via protein kinase C-regulated store-operated Ca(2+) entry. Melamine also caused Ca(2+)-independent cell death.

KEYWORDS:

Ca(2+); Cell death; Human prostate cancer cells; Melamine

PMID:
25305741
DOI:
10.1016/j.etap.2014.09.013
[Indexed for MEDLINE]

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