Lindane-Induced Generation of Reactive Oxygen Species and Depletion of Glutathione Do Not Result in Necrosis in Renal Distal Tubule Cells

Details

• Personal Author:
  Piskac-Collier AL ; Smith MA
• Description:
  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. [Description provided by NIOSH]
• Subjects:
  Environmental Monitoring Hazardous Substances Insecticides Kidney Diseases Occupational Health Oxidants Risk Assessment Safety Urogenital Diseases Urogenital System
• 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

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• ISSN:
  1528-7394
• Document Type:
  Text
• Funding:
  Grant
• Genre:
  Journal Article
• Place as Subject:
  OSHA Region 6 ; Texas
• CIO:
  National Institute for Occupational Safety and Health (NIOSH)
• Topic:
  Workplace Safety & Health
• Location:
  North America
• Volume:
  72
• Issue:
  19
• NIOSHTIC Number:
  nn:20036323
• Citation:
  J Toxicol Environ Health A 2009 Jan; 72(19):1160-1167
• Contact Point Address:
  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
• Email:
  acollier@mdanderson.org
• Federal Fiscal Year:
  2009
• Performing Organization:
  University of Texas Health Science Center, Houston
• Peer Reviewed:
  True
• Start Date:
  20050701
• Source Full Name:
  Journal of Toxicology and Environmental Health, Part A: Current Issues
• End Date:
  20250630
• Collection(s):
  National Institute for Occupational Safety and Health
• Main Document Checksum:
  urn:sha-512:49b7372c57d4d2a312613325a44e8d021f9ebbf0e297dd33ac7f5cb2228d40df1d68fe33ece82fe8f1c80865588e61652035fbcb6674fb54480405c1e7c1fba3
• Download URL:
  https://stacks.cdc.gov/view/cdc/187795/cdc_187795_DS1.pdf
• File Type:
  [PDF - 814.86 KB ]