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The protection of selenium on ROS mediated-apoptosis by mitochondria dysfunction in cadmium-induced LLC-PK(1) cells.
Toxicol In Vitro. 2009 Mar; 23(2):288-94.TV

Abstract

Selenium, an essential trace element, showed the significant protective effects against liver and kidney damage induced by some heavy metals. However, the mechanism how selenium suppresses cadmium (Cd)-induced cytotoxicity remains unclear. In this study, we investigated the protective mechanism of selenium on Cd-induced apoptosis in LLC-PK(1) cells via reactive oxygen species (ROS) and mitochondria linked signal pathway. Studies of PI and Annexin V dual staining analysis demonstrated that 20 microM Cd-induced apoptosis as early as 18 h. A concomitant by the generation of ROS, the loss of mitochondrial membrane potential, cytochrome c (cyt c) release, activation of caspase-9, -3 and regulation of Bcl-2 and Bax were observed. N-acetylcysteine (NAC, 500 microM), a free radical scavenger, was used to determine the involvement of ROS in Cd-induced apoptosis. During the process, selenium played the same role as NAC. The anti-apoptosis exerted by selenium involved the blocking of Cd-induced ROS generation, the inhibition of Cd-induced mitochondrial membrane potential collapse, the prevention of cyt c release, subsequent inhibition of caspase activation and the changed level of Bcl-2 and Bax. Taken together, we concluded that Cd-induced apoptosis was mediated by oxidative stress and selenium produced a significant protection against Cd-induced apoptosis in LLC-PK(1) via ameliorating the mitochondrial dysfunction.

Authors+Show Affiliations

Department of Nutrition and Food Hygiene, Nanjing Medical University, 140 Han-zhong Road, Nanjing 210029, The People's Republic of China.No affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

19135140

Citation

Zhou, Yi-Jing, et al. "The Protection of Selenium On ROS Mediated-apoptosis By Mitochondria Dysfunction in Cadmium-induced LLC-PK(1) Cells." Toxicology in Vitro : an International Journal Published in Association With BIBRA, vol. 23, no. 2, 2009, pp. 288-94.
Zhou YJ, Zhang SP, Liu CW, et al. The protection of selenium on ROS mediated-apoptosis by mitochondria dysfunction in cadmium-induced LLC-PK(1) cells. Toxicol In Vitro. 2009;23(2):288-94.
Zhou, Y. J., Zhang, S. P., Liu, C. W., & Cai, Y. Q. (2009). The protection of selenium on ROS mediated-apoptosis by mitochondria dysfunction in cadmium-induced LLC-PK(1) cells. Toxicology in Vitro : an International Journal Published in Association With BIBRA, 23(2), 288-94. https://doi.org/10.1016/j.tiv.2008.12.009
Zhou YJ, et al. The Protection of Selenium On ROS Mediated-apoptosis By Mitochondria Dysfunction in Cadmium-induced LLC-PK(1) Cells. Toxicol In Vitro. 2009;23(2):288-94. PubMed PMID: 19135140.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - The protection of selenium on ROS mediated-apoptosis by mitochondria dysfunction in cadmium-induced LLC-PK(1) cells. AU - Zhou,Yi-Jing, AU - Zhang,Shi-Ping, AU - Liu,Chang-Wei, AU - Cai,Yun-Qing, Y1 - 2008/12/24/ PY - 2008/07/14/received PY - 2008/11/18/revised PY - 2008/12/11/accepted PY - 2009/1/13/entrez PY - 2009/1/13/pubmed PY - 2009/4/15/medline SP - 288 EP - 94 JF - Toxicology in vitro : an international journal published in association with BIBRA JO - Toxicol In Vitro VL - 23 IS - 2 N2 - Selenium, an essential trace element, showed the significant protective effects against liver and kidney damage induced by some heavy metals. However, the mechanism how selenium suppresses cadmium (Cd)-induced cytotoxicity remains unclear. In this study, we investigated the protective mechanism of selenium on Cd-induced apoptosis in LLC-PK(1) cells via reactive oxygen species (ROS) and mitochondria linked signal pathway. Studies of PI and Annexin V dual staining analysis demonstrated that 20 microM Cd-induced apoptosis as early as 18 h. A concomitant by the generation of ROS, the loss of mitochondrial membrane potential, cytochrome c (cyt c) release, activation of caspase-9, -3 and regulation of Bcl-2 and Bax were observed. N-acetylcysteine (NAC, 500 microM), a free radical scavenger, was used to determine the involvement of ROS in Cd-induced apoptosis. During the process, selenium played the same role as NAC. The anti-apoptosis exerted by selenium involved the blocking of Cd-induced ROS generation, the inhibition of Cd-induced mitochondrial membrane potential collapse, the prevention of cyt c release, subsequent inhibition of caspase activation and the changed level of Bcl-2 and Bax. Taken together, we concluded that Cd-induced apoptosis was mediated by oxidative stress and selenium produced a significant protection against Cd-induced apoptosis in LLC-PK(1) via ameliorating the mitochondrial dysfunction. SN - 0887-2333 UR - https://www.unboundmedicine.com/medline/citation/19135140/The_protection_of_selenium_on_ROS_mediated_apoptosis_by_mitochondria_dysfunction_in_cadmium_induced_LLC_PK_1__cells_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0887-2333(08)00296-8 DB - PRIME DP - Unbound Medicine ER -