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Lindane-Induced generation of reactive oxygen species and depletion of glutathione do not result in necrosis in renal distal tubule cells.

Authors
Piskac-Collier-AL; Smith-MA
Source
J Toxicol Environ Health, A 2009 Jan; 72(19):1160-1167
NIOSHTIC No.
20036323
Abstract
Lindane is a chlorinated hydrocarbon pesticide, currently used in prescription shampoos and lotions to treat scabies and lice infestations. Lindane is known to be nephrotoxic; however, the mechanism of action is not well understood. In other organ systems, lindane produces cellular damage by generation of free radicals and oxidative stress. Morphological changes were observed in lindane-treated Madin-Darby canine kidney (MDCK) cells indicative of apoptosis. Lindane treatment induced time-dependent reactive oxygen species (ROS) generation. Onset of ROS generation correlated with an initial increase in total glutathione (GSH) levels above control values, with a subsequent decline in a time-dependent manner. This decline may be attributed to quenching of free radicals by GSH, thereby decreasing the cellular stores of this antioxidant. Necrotic injury was assessed by measuring lactate dehydrogenase (LDH) leakage from the cell after lindane exposure. No significant LDH leakage was noted for all concentrations tested over time. Generation of ROS and alterations in cellular protective mechanisms did not result in necrotic injury in MDCK cells, which corresponds with our morphological findings of lindane-induced apoptotic changes as opposed to necrosis in MDCK cells. Thus, lindane exposure results in oxidative damage and alterations in antioxidant response in renal distal tubule cells, followed by cell death not attributed to necrotic injury.
Keywords
Cell-biology; Cell-damage; Cell-metabolism; Cellular-reactions; Exposure-assessment; Exposure-levels; Exposure-methods; Hazardous-materials; Kidney-damage; Nephrotoxins; Oxidative-metabolism; Pesticides; Pollution; Renal-toxicity; Risk-analysis; Statistical-analysis
Contact
Amanda L. Piskac-Collier, Department of Epidemiology, Unit 1005, The University of Texas M. D. Anderson Cancer Center, 1515 Holcombe Boulevard, Houston, TX 77030, USA
CODEN
JTEHD6
Publication Date
20090101
Document Type
Journal Article
Email Address
acollier@mdanderson.org
Funding Type
Grant
Fiscal Year
2009
NTIS Accession No.
NTIS Price
Identifying No.
Grant-Number-T42-OH-008421
Issue of Publication
19
ISSN
1528-7394
Source Name
Journal of Toxicology and Environmental Health, Part A: Current Issues
State
TX
Performing Organization
University of Texas, Health Science Center, Houston, Texas
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