Author: Kang Kyung-Sun Lee Yong-Soon Kim Hyung-Sub Kim Sung Hoon
Publisher: Taylor & Francis Ltd
ISSN: 1087-2620
Source: Journal of Toxicology and Environmental Health, Vol.65, Iss.5-6, 2002-03, pp. : 447-459
Disclaimer: Any content in publications that violate the sovereignty, the constitution or regulations of the PRC is not accepted or approved by CNPIEC.
Abstract
Di-(2-ethylhexyl) phthalate (DEHP) has been studied on gap junctional intercellular communication (GJIC) and apoptosis in cultured normal mouse Sertoli cells. Since the inhibition of GJIC and programmed cell death or apoptosis play important roles in tumor promotion and developmental toxicity, it has been hypothesized that tumor promoters may inhibit apoptosis by blocking GJIC. The results showed that the most significant downregulation of GJIC was detected at 9 h after DEHP treatment. However, a significant concentration-dependent pattern was not observed at concentrations of 100 and 500 µ
Related content
By Kamendulis Lisa M. Isenberg Jason S. Smith Jacqueline H. Pugh George Lington Arthur W. Klaunig James E.
Journal of Toxicology and Environmental Health, Vol. 65, Iss. 8, 2002-04 ,pp. :
By Jansen L. Mesnil M. Koeman J. Jongen W.
Environmental Toxicology and Pharmacology, Vol. 1, Iss. 3, 1996-05 ,pp. :
Journal of Toxicology and Environmental Health, Vol. 69, Iss. 9, 2006-05 ,pp. :