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Comparative studies on lipid peroxidation and DNA-single strand breaks induced by lindane, DDT, chlordane and endrin
Abstract:
1. A variety of structurally dissimilar polyhalogenated cyclic hydrocarbons produce similar toxic effects. The molecular mechanisms involved in the production of these toxic manifestations is not known. 2. We have proposed that reactive oxygen species may be involved, and have therefore examined the time-dependent effects of lindane (30 mg/kg), DDT (40 mg/kg), chlordane (120 mg/kg), and endrin (4.5 mg/kg) on the production of hepatic mitochondrial and microsomal lipid peroxidation and DNA single strand breaks, two indices of oxidative stress. 3. All four xenobiotics resulted in significant increases in hepatic lipid peroxidation and DNA damage. Earliest (6 hr) increases in both lipid peroxidation and DNA damage were observed following lindane administration. Time-dependent increases in both parameters were observed following endrin administration. 4. Maximum increases in DNA single strand breaks of 2.8- and 2.5-fold were observed 12 hr after DDT and chlordane administration, respectively, while a 4.4-fold increase was observed 24 hr after endrin administration. 5. The results demonstrate that the four structurally dissimilar polyhalogenated hydrocarbons produce oxidative tissue damage which may contribute to the toxic manifestations of these xenobiotics, and exhibit different toxicokinetic properties.
Insights
Structurally dissimilar polyhalogenated hydrocarbons cause similar toxic effects through oxidative stress. This study examined their impact on hepatic lipid peroxidation and DNA damage, revealing their contribution to xenobiotic toxicity.
Area of Science:
- Environmental Toxicology
- Molecular Toxicology
- Biochemistry
Background:
- Polyhalogenated cyclic hydrocarbons (PHCs) exhibit similar toxic effects despite structural differences.
- The underlying molecular mechanisms of PHC toxicity remain largely unknown.
- Reactive oxygen species (ROS) are hypothesized to play a role in PHC-induced toxicity.
Purpose of the Study:
- To investigate the time-dependent effects of specific PHCs on oxidative stress markers.
- To assess the induction of hepatic mitochondrial and microsomal lipid peroxidation by PHCs.
- To evaluate the generation of DNA single-strand breaks as an indicator of oxidative damage.
Main Methods:
- Administration of lindane, DDT, chlordane, and endrin to experimental subjects.
- Measurement of hepatic lipid peroxidation levels over time.
- Quantification of DNA single-strand breaks in liver tissue.
Main Results:
- All four tested PHCs significantly increased hepatic lipid peroxidation and DNA damage.
- Lindane induced the earliest increases in both parameters (6 hours).
- Endrin exposure resulted in time-dependent increases in lipid peroxidation and DNA damage, with a 4.4-fold increase in DNA breaks at 24 hours.
Conclusions:
- The studied PHCs induce oxidative tissue damage, contributing to their overall toxicity.
- The findings support the involvement of oxidative stress in the toxic mechanisms of these xenobiotics.
- Different PHCs exhibit distinct toxicokinetic properties influencing their damaging effects.