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

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.

Lithium as a prooxidant? A possible protective role of selenium – in vitro study

“…In cells incubated in the presence of As 2 O 3 (100 μM -IC 50 concentration for 10, 20 or 40 h) decreased GPx activity was observed. After 10 and 20 h, in cells preincubated with selenium (1, 5 or 10 μM) for 2 h this effect was alleviated by all doses, whereas after 40 h the higher doses proved to be entirely ineffective [6].…”

“…The outcomes of research on its possible protective properties against prooxidative processes have seemed to be promising and encouraging. Inorganic selenium (sodium selenite) has been found to prevent oxidative stress caused by methamphetamine in neuronal cells [5] and by As 2 O 3 in fish hepatoma cells [6], as well as t-butyl hydroperoxide-induced DNA damage in human mesenchymal stromal cells [7]. Other forms (organic compounds and nanoparticles) of selenium have also been studied and the research has revealed the dependence of the effects on the used form [3,[8][9][10].…”

Protective effects of Selenium and/or Melatonin against Cadmium Chloride induced Chromosomal aberrations in Swiss Albino mice Mus musculus BALB/c

“…Cadmium is known to produce DNA damage and lipid peroxide in vitro and in vivo as well as selenium provides a protective effect against cadmium induced genotoxicity (Hurná et al, 1997). Selenium has ability to increase glutathione peroxidase activity in the elimination of peroxide radicals, thereby providing significant protection against genotoxicity of chemical that induced oxidative DNA damage and apoptosis in aquatic organism (Selvaraj., et al 2012). Cadmium chloride induced their genotixicity through the induction of oxidative stress, while melatonin reduces this effect by detoxification of oxygen and nitrogen-based free radicals and related non-radical products (Jahangir et al 2006;Reiter et al, 2007Reiter et al, , 2010.…”

Anticytotoxic and Radical Scavenging Activities of Acer tegmentosum Maxim Stem Extracts

“…합물은 반응산소종(reactive oxygen species, ROS) 생 성과 세포독성을 증가시켰고, 항산화물질들은 비소에 의 한 산화스트레스 효과를 억제시켰다 (Cha et al, 2006;Soria et al, 2010;Selvaraj et al, 2012). 또한, 동물실 험에서 비소화합물은 간 독성과 간 지질과산화를 촉진시 켰고, 혈중 및 간 GSH 수준을 감소시켰으며, 반면에 페 놀성 화합물은 비소에 의한 독성효과를 억제시켰다고 보 고된 바 있어 (Gao et al, 2013), 비소의 독성효과는 적어 도 산화스트레스에 의한 것으로 알려져 있다.…”