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Nanoplastic-Induced Liver Damage Was Alleviated by Maltol via Enhancing Autophagic Flow: An In Vivo and In Vitro Study

Journal of Agricultural and Food Chemistry 2024 8 citations ? Citation count from OpenAlex, updated daily. May differ slightly from the publisher's own count. Score: 55 ? 0–100 AI score estimating relevance to the microplastics field. Papers below 30 are filtered from public browse.
Ying Liang, Ying Liang, Zi Wang, Deyang Huo, Junnan Hu, Lingjie Song, Xiaochi Ma, Shuang Jiang, Wei Li

Summary

Researchers found that nanoplastic exposure caused liver damage in mice through oxidative stress, cell death, and impaired cellular recycling processes. They then tested maltol, a compound derived from red ginseng, and found it significantly reduced the liver damage by restoring healthy autophagy and reducing oxidative stress. The study suggests that natural compounds like maltol could potentially help protect the liver from the harmful effects of nanoplastic accumulation.

Body Systems
Models
Study Type In vivo

In recent years, there has been a growing concern regarding health issues arising from exposure to nanoplastics (Nps) in the natural environment. The Nps bioaccumulate within the body via the circulatory system and accumulate in the liver, resulting in damage. Previous studies have demonstrated that maltol, derived from red ginseng (Panax ginseng C.A. Meyer) as a Maillard product, exhibits hepatoprotective effects by alleviating liver damage caused by carbon tetrachloride or cisplatin. In order to explore the specific mechanism of maltol in improving hepatotoxicity induced by Nps, mice exposed to 100 mg/kg Nps were given maltol at doses of 50 and 100 mg/kg, respectively. The results showed that Nps induced an increase in the levels of liver apoptotic factors BAX and cytochrome c, a decrease in the levels of the autophagy key gene LC3 II/I, and an increase in P62. It also caused oxidative stress by affecting the Nrf2/HO-1 pathway, and a decrease in GPX4 protein expression suggested the occurrence of ferroptosis. However, treatment with maltol significantly improved these changes. In addition, maltol (2, 4, and 8 μM) also protected human normal liver L02 cells from Np (400 μg/mL)-induced damage. Our data suggest that maltol could ameliorate Np-induced L02 cytotoxicity by reducing autophagy-dependent oxidative stress, exhibiting similar protective effects in vitro as in vivo. This study helps shed light on the specific molecular mechanism of Np-induced hepatotoxicity. For the first time, we studied the protective effect of maltol on Np-induced liver injury from multiple perspectives, expanding the possibility of treatment for diseases caused by environmental pollutants.

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