AI Article Synopsis
- The consumption of fish poses a risk of methylmercury (MeHg) exposure while also providing beneficial omega-3 fatty acids like DHA.
- Epidemiological studies hint that DHA can counteract the neurotoxic effects of MeHg, though the exact mechanism remains unclear.
- Research showed that DHA pretreatment reduced MeHg-induced cell damage by inhibiting reactive oxygen species and was linked to the activation of certain receptor pathways, highlighting DHA’s protective role against neurotoxicity.
Article Abstract
The consumption of fish now involves a risk of methylmercury (MeHg) exposure but also provides the benefit of ω-3 polyunsaturated fatty acids (ω-3 PUFAs) such as docosahexaenoic acid (DHA). Some epidemiological studies have suggested that the intake of DHA can alleviate the neurotoxicity of MeHg, but the underlying mechanism is not known. Herein, we observed that pretreatment with 0.1-1 µM DHA suppressed MeHg-induced cytotoxicity in human neuroblastoma (SH-SY5Y) cells and mouse primary neuronal cells. These effects of DHA were canceled in the presence of the retinoid X receptor (RXR) antagonist UVI3003. An RXR agonist, bexarotene, suppressed the cytotoxicity of MeHg. DHA also suppressed the MeHg-induced production of reactive oxygen species (ROS) via an induction of antioxidant genes ( and ). Pretreatment with DHA did not change the incorporation of MeHg. We showed previously that in the brain, the intake of DHA increased the level of 19,20-DHDP, which is the metabolite produced by cytochrome P450 and soluble epoxide hydrolase from DHA. In the present study, we observed that 19,20-DHDP also suppressed neurotoxicity from MeHg. These results indicate that DHA and its metabolites have a protective role in MeHg-induced neurotoxicity.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8004243 | PMC |
| http://dx.doi.org/10.3390/ijms22063213 | DOI Listing |
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