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Selenite causes cytotoxicity in rainbow trout (Oncorhynchus mykiss) hepatocytes by inducing oxidative stress.
Toxicol In Vitro. 2009 Oct; 23(7):1249-58.TV

Abstract

Selenium is an essential micronutrient to freshwater fish, but can be very toxic at slightly above the threshold level. The liver is known to be the major site of selenium accumulation and metabolism in fish. Recent evidence from mammalian systems suggests that oxidative damage is an important mechanism of selenium toxicity; however this phenomenon has not been investigated in-depth in fish, either in vivo or in vitro. Therefore, the present study was designed to investigate whether selenium (as selenite) exposure causes cytotoxicity in fish by inducing oxidative stress. We used isolated hepatocytes in primary culture from freshwater rainbow trout (Oncorhynchus mykiss) as the model in vitro experimental system. The 24h LD(50) of selenite to trout hepatocytes was found to be 587 microM. In order to evaluate the dose-dependent response patterns of various oxidative stress parameters, the trout hepatocytes were exposed to three different doses of selenite [50, 100 and 200 microM (corresponding to approximately 10%, 20% and 35% of 24h LD(50))] in addition to control (0 microM of selenite) for 24h. We observed an induction of catalase (CAT) and superoxide dismutase (SOD) activities at 50 and 100 microM of selenite exposure, but not at 200 microM, relative to the control. In contrast, the induction of glutathione peroxidase (GPx) activity was recorded at 100 and 200 microM exposure doses, but not at 50 microM. We also demonstrated that selenite exposure (100-200 microM) increased intracellular ROS formation at an early stage (2h). The reduced to oxidized glutathione ratio (GSH:GSSG) decreased sharply with increasing selenite dose, indicating the loss of cellular reducing capacity. The cellular lipid peroxidation tended to increase with increasing selenite exposure dose, indicating the occurrence of membrane damage. A 20-40% decrease in cell viability was observed at 100 and 200 microM of selenite exposure. The increase in cell death was associated with a significant increase of caspase-3/7 activity, suggesting the induction of apoptosis. Overall, the present study suggests that selenite exposure at high level causes oxidative damage to trout hepatocytes, probably by inducing the imbalance of intracellular glutathione (GSH) redox.

Authors+Show Affiliations

Department of Biology, University of Saskatchewan, Saskatoon, Canada.No affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

19651203

Citation

Misra, Sougat, and Som Niyogi. "Selenite Causes Cytotoxicity in Rainbow Trout (Oncorhynchus Mykiss) Hepatocytes By Inducing Oxidative Stress." Toxicology in Vitro : an International Journal Published in Association With BIBRA, vol. 23, no. 7, 2009, pp. 1249-58.
Misra S, Niyogi S. Selenite causes cytotoxicity in rainbow trout (Oncorhynchus mykiss) hepatocytes by inducing oxidative stress. Toxicol In Vitro. 2009;23(7):1249-58.
Misra, S., & Niyogi, S. (2009). Selenite causes cytotoxicity in rainbow trout (Oncorhynchus mykiss) hepatocytes by inducing oxidative stress. Toxicology in Vitro : an International Journal Published in Association With BIBRA, 23(7), 1249-58. https://doi.org/10.1016/j.tiv.2009.07.031
Misra S, Niyogi S. Selenite Causes Cytotoxicity in Rainbow Trout (Oncorhynchus Mykiss) Hepatocytes By Inducing Oxidative Stress. Toxicol In Vitro. 2009;23(7):1249-58. PubMed PMID: 19651203.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Selenite causes cytotoxicity in rainbow trout (Oncorhynchus mykiss) hepatocytes by inducing oxidative stress. AU - Misra,Sougat, AU - Niyogi,Som, Y1 - 2009/08/03/ PY - 2009/04/07/received PY - 2009/07/14/revised PY - 2009/07/28/accepted PY - 2009/8/5/entrez PY - 2009/8/5/pubmed PY - 2009/12/16/medline SP - 1249 EP - 58 JF - Toxicology in vitro : an international journal published in association with BIBRA JO - Toxicol In Vitro VL - 23 IS - 7 N2 - Selenium is an essential micronutrient to freshwater fish, but can be very toxic at slightly above the threshold level. The liver is known to be the major site of selenium accumulation and metabolism in fish. Recent evidence from mammalian systems suggests that oxidative damage is an important mechanism of selenium toxicity; however this phenomenon has not been investigated in-depth in fish, either in vivo or in vitro. Therefore, the present study was designed to investigate whether selenium (as selenite) exposure causes cytotoxicity in fish by inducing oxidative stress. We used isolated hepatocytes in primary culture from freshwater rainbow trout (Oncorhynchus mykiss) as the model in vitro experimental system. The 24h LD(50) of selenite to trout hepatocytes was found to be 587 microM. In order to evaluate the dose-dependent response patterns of various oxidative stress parameters, the trout hepatocytes were exposed to three different doses of selenite [50, 100 and 200 microM (corresponding to approximately 10%, 20% and 35% of 24h LD(50))] in addition to control (0 microM of selenite) for 24h. We observed an induction of catalase (CAT) and superoxide dismutase (SOD) activities at 50 and 100 microM of selenite exposure, but not at 200 microM, relative to the control. In contrast, the induction of glutathione peroxidase (GPx) activity was recorded at 100 and 200 microM exposure doses, but not at 50 microM. We also demonstrated that selenite exposure (100-200 microM) increased intracellular ROS formation at an early stage (2h). The reduced to oxidized glutathione ratio (GSH:GSSG) decreased sharply with increasing selenite dose, indicating the loss of cellular reducing capacity. The cellular lipid peroxidation tended to increase with increasing selenite exposure dose, indicating the occurrence of membrane damage. A 20-40% decrease in cell viability was observed at 100 and 200 microM of selenite exposure. The increase in cell death was associated with a significant increase of caspase-3/7 activity, suggesting the induction of apoptosis. Overall, the present study suggests that selenite exposure at high level causes oxidative damage to trout hepatocytes, probably by inducing the imbalance of intracellular glutathione (GSH) redox. SN - 1879-3177 UR - https://www.unboundmedicine.com/medline/citation/19651203/Selenite_causes_cytotoxicity_in_rainbow_trout__Oncorhynchus_mykiss__hepatocytes_by_inducing_oxidative_stress_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0887-2333(09)00202-1 DB - PRIME DP - Unbound Medicine ER -