Trichloroethylene (TCE), a common water pollutant linked to Parkinson’s Disease (PD), induces dopaminergic neurodegeneration. L-Theanine (L-Th) was explored as a potential treatment for TCE-induced PD due to its previously elucidated neuroprotective properties. Cell viability, cytotoxicity, and cell density were evaluated using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) cell viability assay (n=8), lactate dehydrogenase (LDH) assay (n=4), and cell image analysis (n=6), respectively. GT1-7 and SK-N-SH cells served as dopaminergic and neuronal cell models, respectively. In GT1-7 cells, L-Th 600 μM diminished TCE 1000 μM-induced cell death and TCE 1000 μM-induced LDH release by 81% (p<0.001) and 38% (p<0.001), respectively, after 48 h. L-Th also did not significantly impact LDH leakage in healthy GT1-7 cells. In SK-N-SH cells, L-Th 600 μM attenuated TCE 100 μM’s neurodegenerative effects by increasing cellular density and cellular area by 118% (p<0.01) and 170% (p<0.001), respectively, after 24 h. L-Th’s mitigation of TCE’s neurotoxic and neurodegenerative effects in dopaminergic neurons can prevent dopaminergic neurodegeneration: linked to PD onset. L-Th’s ability to preserve healthy GT1-7 cells indicates that L-Th not neurotoxic in vitro. This research marks the identification of the first potential treatment for TCE-induced PD. Future investigations should explore the mechanism of L-Th and TCE’s interactions.
Keywords: Trichloroethylene, environmental toxin, L-Theanine, Parkinson’s disease, neurodegeneration.
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