Combined effect of polystyrene microplastics and cadmium on rat blood-testis barrier integrity and sperm quality.

The harmful effects of microplastics and Cd on the testicular activity of sexually mature rats are here documented. Oral treatment with both substances caused testicular impairment that was evidenced by histological and biomolecular alterations, such as MP accumulation in the seminiferous epithelium, imbalance of oxidative status, and reduced sperm quality. Importantly, the cytoarchitecture of the blood-testis barrier was compromised, as revealed by the down-regulation of protein levels of structural occludin, Van Gogh-like protein 2, and connexin 43 and activation of regulative kinases proto-oncogene tyrosine-protein kinase and focal adhesion kinase. Interestingly, for the first time, MPs are reported to activate the autophagy pathway in germ cells, to reduce damaged organelles and molecules, probably in an attempt to avoid apoptosis. Surprisingly, the results obtained with the simultaneous Cd + MPs treatment showed more harmful effects than those produced by MPs alone but less severe than with Cd alone. This might be due to the different ways of administration to rats (oral gavage for MPs and in drinking water for Cd), which might favor the adsorption, in the gastrointestinal tract, of Cd by MPs, which, by exploiting the Trojan horse effect, reduces the bioavailability of Cd.

Exposure to microplastics leads to a defective ovarian function and change in cytoskeleton protein expression in rat.

Microplastics (MPs) are ubiquitous environmental contaminants; through their physicochemical properties, they can have potentially negative effects on the environment as well as on animal and human health. Studies addressing the toxicity of MPs on mammalian female reproduction are almost absent. Thus, the main objective of the present study was to assess the impact of oral exposure, during four estrous cycles, of 5 µm polystyrene-type microplastics (PS-MPs) on ovarian function in rats. Particles of PS-MPs were detected in the duodenum and, for the first time, in the different compartments of the ovarian tissue. The toxicity of accumulated PS-MPs was manifested by the reduced relative ovarian weights, by the alteration in the folliculogenesis and in the estrous cycle duration, and by the reduced serum concentration of estradiol. The defective ovarian function following PS-MP treatment might be due to the induction of oxidative stress, which has been proved by an increased malondialdehyde (MDA) concentration and an increased superoxide dismutase (SOD) and catalase (CAT) activities as well as a decreased protein sulfhydryl (PSH) level in the rat ovary. Importantly, by immunofluorescence and RT-PCR, we demonstrated a significant decrease in the expression of cytoskeletal proteins: α-tubulin and disheveled-associated activator of morphogenesis (DAAM-1) in the ovary of rats exposed to PS-MPs at proteomic and transcriptomic levels. Our results uncovered, for the first time, the distribution and accumulation of PS-MPs across rat ovary, revealed a significant alteration in some biomarkers of the ovarian function, and highlighted the possible involvement of MP-induced disturbance of cytoskeleton in these adverse effects.