Modulation of the genotoxicity of pesticides reacted with redox-modified smectite clay.
Pesticides are toxic agents intentionally released into the environment; their use raises public health and environmental concerns. In recent years there has been much attention to the biotic degradation of pesticides. Abiotic mechanisms in the soil can contribute to pesticide degradation yet the toxicological impact of such degradation is unclear. This study combines for the first time an investigation into abiotic mechanisms of degradation coupled with toxicological endpoints in mammalian cells. The genotoxicity of three commonly used agricultural pesticides was assessed before and after exposure to redox-modified clay minerals. The objectives of the study were to determine the genotoxicity of 2,4-dichlorophenoxy acetic acid (2,4-D), dicamba, and oxamyl, using single cell gel electrophoresis with Chinese hamster ovary (CHO) cells, and to determine the effect of the iron oxidation state in clay minerals (ferruginous smectite SWa-1) on the genotoxic potency of the pesticides. 2,4-D alone or following reaction with redox-modified clays did not induce DNA damage in CHO cells. Oxamyl alone induced a concentration-dependent increase in genomic DNA damage; however, its genotoxicity declined after reaction with reduced clay minerals. Dicamba was not genotoxic when directly analyzed. When dicamba was reacted with reduced clay, a concentration-dependent increase in genomic DNA damage was observed. This is the first reported case of a pesticide being converted into a genotoxin after exposure to redox-modified smectites. These data introduce a new paradigm on the interaction between redox-modified clays and pesticide-related environmental genotoxicity.
Sorensen
Kara C
KC
Department of Natural Resources and Environmental Sciences, College of Agricultural, Consumer and Environmental Sciences,University of Illinois at Urbana-Champaign, Urbana, Illinois 61801, USA.
Stucki
Joseph W
JW
Warner
Richard E
RE
Wagner
Elizabeth D
ED
Plewa
Michael J
MJ
D015084:2,4-Dichlorophenoxyacetic Acid / Q000633:toxicity; D000538:Aluminum Silicates / Q000737:chemistry*; D000818:Animals; D001673:Biodegradation, Environmental; D016466:CHO Cells; D002219:Carbamates / Q000633:toxicity; D000077215:Clay; D020552:Comet Assay; D006224:Cricetinae; D004249:DNA Damage; D003996:Dicamba / Q000633:toxicity; D004305:Dose-Response Relationship, Drug; D004785:Environmental Pollutants; D006540:Herbicides / Q000737:chemistry; D007501:Iron / Q000737:chemistry / Q000378:metabolism; D008956:Models, Chemical; D009153:Mutagens; D010084:Oxidation-Reduction; D010100:Oxygen / Q000737:chemistry / Q000378:metabolism; D010575:Pesticides / Q000737:chemistry / Q000494:pharmacology / Q000633:toxicity*; D017640:Silicates / Q000737:chemistry*
D000538:Aluminum Silicates; D002219:Carbamates; D004785:Environmental Pollutants; D006540:Herbicides; D009153:Mutagens; D010575:Pesticides; D017640:Silicates; D015084:2,4-Dichlorophenoxyacetic Acid; C033214:Smectite; D007501:Iron; D010100:Oxygen; D003996:Dicamba; C011960:oxamyl; D000077215:Clay