Spinetoram is an important semi-synthetic insecticide extensively applied in agriculture. It is neurotoxic to insects, primarily by acting on acetylcholine receptors (nAChRs). However, few studies have examined the neurotoxicity of spinetoram in human beings. In this study, various concentrations (5, 10, 15, and 20 μM) of spinetoram were employed to expose SH-SY5Y cells in order to study the neurotoxic effects of spinetoram. The results showed that spinetoram exposure markedly inhibited cell viability and induced oxidative stress. It also induced mitochondrial membrane potential collapse (ΔΨm), and then caused a massive opening of the mitochondrial permeability transition pore (mPTP), a decrease in ATP synthesis, and Ca²⁺ overloading. Furthermore, spinetoram exposure induced cellular autophagy, as evidenced by the formation of autophagosomes, the conversion of LC3-I into LC3-II, down-regulation of p62, and up-regulation of beclin-1. In addition, we observed that p-mTOR expression decreased, while p-AMPK expression increased when exposed to spinetoram, indicating spinetoram triggered AMPK/mTOR-mediated autophagy. Complementarily, the effect of spinetoram on neurobehavior was studied using the zebrafish model. After being exposed to different concentrations (5, 10, and 20 μg/mL) of spinetoram, zebrafish showed neurobehavioral irregularities, such as reduced frequency of tail swings and spontaneous movements. Similarly, autophagy was also observed in zebrafish. In conclusion, spinetoram exposure produced potential neurotoxicity through autophagy mediated by mitochondrial damage. The experimental data and results of the neurotoxicity study of spinetoram provided above are intended to serve as reference for its safety assessment.

The invention and use of chelating purification products directed at atmospheric particulate matter 2.5 (PM2.5) are beneficial in preventing cytotoxicity and bodily harm. However, natural plant active compounds that minimize the adverse effect of PM2.5 are rarely reported. Chlorella pyrenoidosa extracts (CPEs), a nutritional supplement derived from Chlorella vulgaris, have been shown to have antioxidant and anti-inflammatory effects. Here, we discovered that CPEs extracted with crushing cell extraction technology can attenuate the negative impacts of PM2.5. Furthermore, CPE intervention can protect against DNA damage and unstable genomic structure due to PM2.5 exposure. Moreover, CPE intervention restored mRNA and protein expression of the DNA misincorporation repair mechanism gene, nudix hydrolase 1 (NUDT1), and 8-oxoguanine DNA glycosylase (OGG1). In vivo damage protection experiments revealed that CPEs reduced PM2.5-induced hepatotoxicity of zebrafish larvae and effectively prevented the death of adult zebrafish exposed to PM2.5. Briefly, CPEs can attenuate cytotoxicity, resist DNA damage, relieve PM2.5-induced hepatotoxicity, and improve cell purification activity, making them ideal for use as a protective factor or functional ingredient in the cosmetics and health food industries.