NDLI: Protective and antioxidant role of selenium on arsenic trioxide–induced oxidative stress and genotoxicity in the fish hepatoma cell line PLHC-1

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Protective and antioxidant role of selenium on arsenic trioxide–induced oxidative stress and genotoxicity in the fish hepatoma cell line PLHC-1

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Selvaraj, Vellaisamy Yeager-Armstead, Mindy Murray, Elizabeth
Description	Country affiliation: United States Author Affiliation: Selvaraj V ( Department of Integrated Science and Technology, Marshall University, Huntington, WV, USA.)
Abstract	In vitro models are useful tools for rapid screening for toxicity, elucidation of mechanisms of toxicity, and understanding complex interactions among environmental toxicants. These evaluations may provide useful information for ecological evaluations if the relationship between in vitro and in vivo effects is established. The present study was undertaken to evaluate the protective effect of selenium on arsenic trioxide $(As_{2}O_{3})–induced$ cytotoxicity, DNA damage, and apoptosis. N-acetylcysteine (NAC), a free radical scavenger, was used to determine the involvement of reactive oxygen species (ROS) in $As_{2}O_{3}-induced$ DNA damage and apoptosis. Poeciliopsis lucida hepatocellular carcinoma line 1 (PLHC-1) cells were pretreated with selenium (1, 5, and 10 µM) and NAC (50 and 100 µM) for 2 h. After pretreatment, cells were exposed to 100 µM of $As_{2}O_{3}$ for 10-, 20-, and 40-h intervals. The $As_{2}O_{3}$ exposure promoted extensive DNA damage and apoptosis compared to control, while selenium- and NAC-pretreated cells improved cell survival rate against $As_{2}O_{3}-induced$ cell death. Improved survival likely resulted from increasing glutathione peroxidase activity and reduction of ROS formation, reduction of mitochondrial membrane potential damage, DNA damage, and caspase-3 activity. During $As_{2}O_{3}$ exposure, selenium played the same role as NAC. The authors conclude that $As_{2}O_{3}-induced$ DNA damage and apoptosis are mediated by oxidative stress and selenium and that, although toxic at higher concentrations, selenium provides significant protection against $As_{2}O_{3}$ effects in PLHC-1 cells. Environ. Toxicol. Chem. 2012; 31: 2861–2869. © 2012 SETAC
File Format	HTM / HTML
ISSN	07307268
Issue Number	12
Volume Number	31
e-ISSN	15528618
Journal	Environmental Toxicology and Chemistry
Language	English
Publisher	Wiley
Publisher Date	2012-12-01
Publisher Place	United States
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Research Support, Non-u.s. Gov't Reactive Oxygen Species Oxidative Stress Toxicity Arsenicals Discipline Environmental Health Acetylcysteine Discipline Toxicology Oxides Free Radical Scavengers Hazardous Substances Dna Damage Journal Article Antioxidants Fishes Membrane Potential, Mitochondrial Caspase 3 Discipline Chemistry Selenium Pharmacology Metabolism Drug Effects Animals Mutagens Cell Line, Tumor Apoptosis
Content Type	Text
Resource Type	Article
Subject	Environmental Chemistry Health, Toxicology and Mutagenesis

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