Diet provides energy and nutrition for human survival, and also provides various joy of taste. Extensive studies have shown that the major components of diet, such as protein, carbohydrate and fat, play important roles in regulating aging and longevity. Whether other dietary ingredients can help prevent aging and extend longevity is a very interesting question. Here based on recent findings, we discussed dietary plant ingredients that can extend longevity by regulation of metabolism, targeting TRP channels, mitophagy, senescence pathways and circadian rhythms. Better understanding of the detailed effects and mechanisms of dietary ingredients on longevity regulation, would be helpful for developing new intervention tools for preventing aging and aging related diseases. Supplementary Information The online version contains supplementary material available at 10.1007/s11130-021-00946-z.
Glutamate excitotoxicity, characterized as excessive glutamate stress, is considered to be involved in cerebral ischaemia, brain trauma, and neurodegenerative diseases such as Parkinson's disease and Alzheimer's disease. Glutamate homeostasis disruption was highlighted in Mn neurotoxicity caused by high levels of Mn. Astrocytes, accounting for approximately 50% of the neuronal cells in the central nervous system and maintain glutamate homeostasis, are sensitive to neurotoxicity induced by Mn exposure. Astrocytes are tightly coupled with gap junctions (GJ), which are comprised of connexins, mainly connexin43 (Cx43). The gap junctional intercellular communication (GJIC) pathway allows small signal molecules, such as glutamate, ATP (adenosine triphosphate, ATP) and tropic factors, etc., to transfer between adjacent cells. Evidence has shown that astrocytes execute the bystander effect during cell death through the GJIC pathway. However, the pathogenic mechanism of the gap junction underlying glutamate neurotoxicity induced by manganese exposure has not been elucidated yet. In the present study, primary astrocytes were cultured and then exposed to different levels of Mn (ranging from 0 to 1000 μM) for 4/16 h to investigate the function of the GJIC in apoptosis induced by Mn. The cellular toxicity was confirmed by cell viability and apoptotic percentage through MTT assay and flow cytometry (FC). The levels of intracellular/extracellular glutamate were measured by high-performance liquid chromatography (HPLC). The fluorescent dye, Lucifer Yellow (LY), was used to assess the status of gap junctions among astrocytes after Mn exposure. The protein/gene expression of major gap junctional forming protein, Cx43, was also investigated. Cell viability was distinctly reduced when exposed to 500 and 1000 μM MnCl compared with control cells at both time points. The percentage of apoptosis was significantly increased among all detected Mn levels (125, 500 and 1000 μM MnCl) of exposure (p < 0.05) with a concentration-dependent manner at either time point. Mn administration for 4/16 h also caused a remarkable intracellular/extracellular glutamate increase in a concentration-dependent manner for extracellular glutamate levels (p < 0.01). Gap junctions were prominently inhibited by Mn with Cx43 protein shown as shortening of the LY dye transfer distance at both time points. In-cell western blot indicated that Mn caused a decrease in Cx43 protein/gene expression in a dose-dependent manner. These results suggested that the gap junction intercellular communication and its forming protein, Cx43, are likely involved in glutamate excitotoxicity induced by Mn exposure.
In recent years, as an emerging pollutant, microplastic (MPs) pollution is gradually becoming a research hotspot.MPs are ubiquitous in the entire ecological environment. Organisms can be exposed to MPs via inhalation or ingestion. In view of the widespread of MPs pollution, the impact of MPs on biology should be further investigated. In previous experiments, we have conducted research on the physiology of Drosophila exposed to polyethylene terephthalate microplastics (PET-MPs). However, will the lifespan of Drosophila be affected under long-term PET-MPs exposure? The analysis of variance analysis of our experimental results indicates that there are significant differences between males and females, F(1, 895) = 68.19, p < 0.001, between PET-MPs concentration, F(3, 895) = 8.11, p < 0.001. There are also significant interactions between sex and MP concentration, F(3, 895) = 4.00, p < 0.01. For Cox and log-rank test, 1 g/L of PET-MPs prolongs the lifespan of male flies. The reason for this phenomenon may be the hormesis effect.
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