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Lycopene againsts the polystyrene microplastics-induced neurotoxicity via modulation of mTOR/Beclin-1 activities in adult male Wistar rats

Clinical Traditional Medicine and Pharmacology 2024 10 citations ? Citation count from OpenAlex, updated daily. May differ slightly from the publisher's own count. Score: 60 ? 0–100 AI score estimating relevance to the microplastics field. Papers below 30 are filtered from public browse.
Mega Obukohwo Oyovwi, Mega Obukohwo Oyovwi, Mega Obukohwo Oyovwi, Ohwin Peggy Ejiro, Rotu Arientare Rume, Ohwin Peggy Ejiro, Rotu Arientare Rume, Tesi P. Edesiri, Tesi P. Edesiri, Tesi P. Edesiri, Tesi P. Edesiri, Benneth Ben‐Azu N. Alexander, N. Alexander, Benneth Ben‐Azu

Summary

Researchers found that lycopene, a natural compound found in tomatoes, protected rat brains from damage caused by polystyrene microplastics. The microplastics caused oxidative stress, disrupted neurotransmitter balance, and triggered harmful cellular processes in the brain, but lycopene treatment reversed many of these effects. This study suggests that antioxidant-rich foods might help protect against the brain-damaging effects of microplastic exposure.

Polymers
Body Systems
Models

Polystyrene microplastics (PS-MPs) pose a significant threat to aquatic ecosystems, causing neuronal toxicity in aquatic species, and Lycopene (LYC), a neuroprotective substance, could potentially mitigate this issue. This study examined the neurotherapeutic benefit of lycopene on the neurochemical status of rats affected by PS-MPs. Twenty Wistar rats were divided into four groups of five rats each: a vehicle group, a PS-MPs treatment group, a PS-MPs + LYC co-treatment group, and an LYC supplementation group. The experiment lasted 56 days, and all substances were administered orally. Neuronal toxicity was evaluated using oxidative stress/neurochemical biomarkers. Lipid peroxidation (LPO), glutathione (GSH), superoxide dismutase (SOD), and catalase (CAT) were measured as indicators of oxidative stress. Nitric Oxide (NO), gamma-aminobutyric acid (GABA), hydroxyl radical ( • OH), ammonia, and glutamate levels were assessed to evaluate neurotransmitter balance. Cathepsin marker enzyme activity was also measured to assess lysosomal function. PS-MPs-treated animals showed increased LPO, NO, • OH, Bcl-2 interacting protein 1 (Beclin-1), ammonia, glutamate, and reduced GABA, Mammalian targets of rapamycin (mTOR), and antioxidant activity in their cerebral cortex. The combination of PS-MPs and Lycopene treatment improved GABA, cathepsin marker enzyme activity, and brain structure, restoring normal neuronal bodies, oval nuclei, and cerebral cortex. Lycopene ameliorated oxidative stress deficits, decreased LPO, NO, • OH, ammonia, and glutamate levels, and restored antioxidant enzyme activity. In conclusion, the findings suggest a potential link between PS-MPs and cognitive dysfunction through neurochemical alterations, while the administration of lycopene mitigated the neurochemical changes brought on by PS-MPs.

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