Regular ArticleLipid Peroxidation and Formation of 8-Hydroxydeoxyguanosine from Acute Doses of Halogenated Acetic Acids
References (0)
Cited by (80)
Associations of urinary dichloroacetic acid and trichloroacetic acid exposure with platelet indices: Exploring the mediating role of blood pressure in the general population
2021, Journal of Hazardous MaterialsCitation Excerpt :Our results suggest that exposure to DCAA and TCAA may alter BP in the general population. Toxicological studies have shown that DCAA and TCAA can induce lipid peroxidation in rodents and produce 8-hydroxydeoxyguanosine (8−OHdG) in mice (Austin et al., 1996). Epidemiological studies further suggested that exposure to DCAA and TCAA during pregnancy may increase maternal oxidative stress biomarkers, 8−OHdG, 4-hydroxy-2-nonenal-mercapturic acid, and 8-iso-prostaglandin F2α (Liu et al., 2020).
Urinary trichloroacetic acid and high blood pressure: A cross-sectional study of general adults in Shijiazhuang, China
2019, Environmental ResearchCitation Excerpt :Furthermore, TCE increases the release of pro-inflammatory cytokines, such as interferon-γ and interleukin-17 (Li et al., 2018). TCAA causes lipid peroxidation and induces increased 8-hydroxydeoxyguanosine formation, which, in turn, may be associated with increased cardiovascular risk (Austin et al., 1996). However, the association between TCAA and blood pressure (BP) has not been studied to date.
Hepatoprotective activity of date fruit extracts against dichloroacetic acid-induced liver damage in rats
2014, Journal of Functional FoodsCitation Excerpt :DCA was metabolized in the cytosol of hepatic cells via reductive dechlorination pathways catalyzed by cytochrome P-450 enzymes, leading to the production of several free radicals that can contribute to the generation of reactive oxygen species (ROS) (Larson & Bull, 1992). The lipid peroxidation resulting from ROS causes oxidative damage to DNA, proteins and lipids (Austin, Parrish, Kinder, & Bull, 1996) and consequently causes organ toxicity. The data in the present study showed that subchronic exposure to DCA at a dose of 0.5 or 2 g/l (33.78 or 131.24 mg/kg) changed body and relative liver weights, conducting to significant decreases in animal growth and production performances.
Trichloroethylene: Mechanistic, epidemiologic and other supporting evidence of carcinogenic hazard
2014, Pharmacology and TherapeuticsCitation Excerpt :Numerous animal studies have demonstrated that TCE is hepatotoxic, as evidenced by the elevation of serum enzymes and bile acids (Hamdan & Stacey, 1993; Ramdhan et al., 2008). A few studies examined TCA- and DCA-induced hepatic oxidative stress and demonstrated small, albeit significant, increases in lipid peroxidation and oxidative DNA damage (Austin et al., 1996; Parrish et al., 1996). This mechanism has not been addressed in humans in vivo or in vitro studies of either TCE or its metabolites.
Protective role of boron on hepatotoxicity and oxidative stress induced by trichloroacetic acid
2023, Environmental Sciences EuropeIs There a Role for Environmental and Metabolic Factors Predisposing to Severe COVID-19?
2020, Hormone and Metabolic Research