Micro- and nanoplastics (MPs/NPs) are among the most widely distributed pollutants in the environment. It has been suggested that exposure to MPs/NPs can trigger toxicity pathways among which inflammation and oxidative stress (OS) play a pivotal role. Once absorbed, MPs/NPs may act locally or access the bloodstream and, following the translocation process, reach several organs and tissues, including the gonads. Notably, MPs/NPs can bioaccumulate in human and murine placenta, opening new scenarios for toxicological evaluations. We review recent studies on the effects of MPs/NPs on the reproductive health in aquatic and terrestrial organisms of both sexes, focusing on the role of OS and the antioxidant defence system failure as the main underlying mechanisms. Alterations in gametogenesis, embryonic and offspring development, and survival have been shown in most studies and often related to a broken redox balance. All these detrimental effects are inversely related to particle size, whereas they are closely linked to shape, plastic polymer type, superficial functionalization, concentration, and time of exposure. To date, the studies provide insights into the health impacts, but no conclusions can be drawn for reproduction toxicity. The main implication of the few studies on antioxidant substances reveals their potential role in mitigating MP-induced toxic effects.

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Microplastics (MPs) are pollutants widely distributed in aquatic ecosystems. MPs are introduced mainly by ingestion acting locally or in organs far from the gastroenteric tract. MPs-induced health consequences for fish species still need to be fully understood. We aimed to investigate the effects of the subchronic oral exposure to polystyrene microplastics (PS-MPs) (1–20 μm) in the gilthead seabreams (Sparus aurata) used as the experimental model. We studied the detrimental impact of PS-MPs (25 and 250 mg/kg b.w./day) on the redox balance and antioxidant status in the intestine using histological analysis and molecular techniques. The research goal was to examine the anterior (AI) and posterior intestine (PI) tracts, characterized by morphological and functional differences. PS-MPs caused an increase of reactive oxygen species and nitrosylated proteins in both tracts, as well as augmented malondialdehyde production in the PI. PS-MPs also differently affected gene expression of antioxidant enzymes (i.e., superoxide dismutase, catalase, glutathione reductase). Moreover, an increased up-regulation of protective heat shock proteins (HSPs) (i.e., hsp70 and hsp90) was observed in PI. Our findings demonstrate that PS-MPs are responsible for oxidative/nitrosative stress and alterations of detoxifying defense system responses with differences in AI and PI of gilthead seabreams.

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Background It is well known that high-fat diet (HFD) feeding causes cardiac inflammation, remodeling, and dysfunction, and that increased fat intake, especially saturated fat, is a major driver of cardiometabolic diseases. Oleoylethanolamide (OEA) is a member of acylethanolamides recognized for its metabolic and anti-inflammatory properties due to the high affinity for different receptors and to its role as a modulator of the endocannabinoid system. OEA effects on the cardiovascular alterations caused by fat overnutrition are still unknown. Purpose The aim of this study was to evaluate the impact of OEA treatment on cardiac metabolic changes induced by HFD in obese mice. Methods Male C57Bl/6J mice were divided into 3 groups: control group (STD) receiving standard chow diet; mice fed with HFD for 20 weeks; HFD group treated with OEA (HFD+OEA 2,5 mg/kg/die i.p.) from week 12 to week 20. Results In HFD mice, OEA treatment reduced body weight measured throughout the experimental period. Before sacrifice, we performed the oral glucose tolerance test (OGTT), where HFD+OEA mice showed an improvement of insulin sensitivity, altered by HFD. HFD feeding led to a significant increase in the production of inflammatory cytokines and chemokines, such as interleukin (IL)-1b, IL-6, the monocyte chemoattractant protein (MCP)1 and the pro-fibrotic marker fibrillin in the cardiac tissue. Conversely, OEA normalized the transcription of the above-mentioned pro-inflammatory mediators in the heart of obese mice. OEA treatment also reduced the gene expressions levels of cardiac fatty acid transporter CD36, that were significantly induced in the heart of HFD-fed mice, and that have been found to be linked to myocardial lipid accumulation. We also evaluated the gene expression levels of the adipokines adiponectin and meteorin-like protein (Metrnl), finding that the increased ventricular expression of both in HFD mice were significantly reduced by OEA. Moreover, OEA treatment induces an increase in AMPK and AKT phosphorylation, whose pathways converge towards the phosphorylation of AS160, a kinase implicated in the translocation of the glucose transporter (GLUT) 4 to the cardiomyocyte membrane, a mechanism involved in the modulation of cardiac glucose metabolism. Since it has been reported that cardiac autophagy is altered in metabolic disorders like obesity, we also studied the effect of OEA in autophagosome formation, and we determined that cardiac protein levels of LC3II, an autophagosomal membrane marker, are markedly increased by OEA treatment. Conclusions Taken together, our results indicate a potential cardioprotective effect of OEA as a molecule able to reduce body weight and body weight gain, to ameliorate glucose disposal improving blood glucose, to restore cardiac metabolic alterations related to obesity, and to decrease proinflammatory and profibrotic markers at cardiac level, induced by HFD. Funding Acknowledgement Type of funding sources: Public Institution(s). Main funding source(s): Fondo de Investigationes Sanitarias, Instituto de Salud Carlos III