Mancozeb is a widely used fungicide, considered to be an endocrine disruptor. In vivo and in vitro studies evidenced its reproductive toxicity on mouse oocytes by altering spindle morphology, impairing oocyte maturation, fertilization, and embryo implantation. Mancozeb also induces dose-dependent toxicity on the ultrastructure of mouse granulosa cells, including chromatin condensation, membrane blebbing, and vacuolization. We evaluated the effects on the ultrastructure of mouse oocytes isolated from cumulus-oocyte complexes (COCs), exposed in vitro to increasing concentrations of mancozeb. COCs were matured in vitro with or without (control) low fungicide concentrations (0.001–1 μg/mL). All mature oocytes were collected and prepared for light and transmission electron microscopy. Results showed a preserved ultrastructure at the lowest doses (0.001–0.01 μg/mL), with evident clusters of round-to-ovoid mitochondria, visible electron-dense round cortical granules, and thin microvilli. Mancozeb concentration of 1 μg/mL affected organelle density concerning controls, with a reduction of mitochondria, appearing moderately vacuolated, cortical granules, and microvilli, short and less abundant. In summary, ultrastructural data revealed changes mainly at the highest concentration of mancozeb on mouse oocytes. This could be responsible for the previously described impaired capability in oocyte maturation, fertilization, and embryo implantation, demonstrating its impact on the reproductive health and fertility.

Since the Fukushima Daiichi Nuclear Power Plant (FDNPP) accident, great attention has been paid to the impact of chronic low-dose-rate (LDR) radiation exposure on biological systems. The reproductive system is sensitive to radiation, with implications connected to infertility. We investigated the testis ultrastructure of the wild large Japanese field mouse (Apodemus speciosus) from three areas contaminated after the FDNPP accident, with different levels of LDR radiation (0.29 µSv/h, 5.11 µSv/h, and 11.80 µSv/h). Results showed good preservation of the seminiferous tubules, comparable to the unexposed animals (controls), except for some ultrastructural modifications. Increases in the numerical density of lipid droplet clusters in spermatogenic cells were found at high levels of LDR radiation, indicating an antioxidant activity rising due to radiation recovery. In all groups, wide intercellular spaces were found between spermatogenic cells, and cytoplasmic vacuolization increased at intermediate and high levels and vacuolated mitochondria at the high-level. However, these findings were also related to the physiological dynamics of spermatogenesis. In conclusion, the testes of A. speciosus exposed to LDR radiation associated with the FDNPP accident showed a normal spermatogenesis, with some ultrastructural changes. These outcomes may add information on the reproductive potential of mammals chronically exposed to LDR radiation.

Zona pellucida, a dense cross-linked network of glycoprotein filaments, evidences a smart morpho-structural change through self-extension/-contraction/-bending of the interconnected filaments capable of sizing/shaping the overall extracellular membrane at different oocyte stages.

Micro- and nanoplastics (MNPs) are ubiquitous environmental pollutants recognized as emerging and relevant risk factors for numerous human diseases, including cardiovascular diseases. MNPs enter the human body through ingestion, inhalation, and dermal penetration, and their toxicity varies according to size, shape, and chemical composition, most notably between microplastics (>1 µm) and nanoplastics (<1 µm), which differ in cellular uptake mechanisms and biodistribution. Recent evidence has confirmed their presence in cardiac and vascular tissues, raising significant concerns about their potential impact on human health. This review summarizes current knowledge on MNP exposure sources, physicochemical properties, and systemic bioavailability, with a particular emphasis on the mechanisms of transport that facilitate their deposition within the myocardium and vasculature. It further addresses a broad spectrum of cardiotoxic effects, including oxidative stress, mitochondrial injury, immune activation, ion channel disruption, cell death, and fibrosis. Endothelial dysfunction, vascular injury, and pro-atherogenic activity are also discussed. In addition to outlining existing detection techniques and emerging in vitro models, the review highlights initial steps toward the development of preventive strategies. Concluding with key knowledge gaps and future research directions, this article underscores the urgent need for standardized measurement tools, deeper insights into damage mechanisms, and clinical interventions to prevent MNP-induced cardiovascular diseases.

The variation in reproductive age among individuals is significant, with many cases of infertility involving premature ovarian aging. This issue, combined with the societal trend of delaying childbearing, leads to age-related ovarian dysfunction. Ovarian aging is related to a decline of ovarian reserve, as oocyte quantity, quality, and precocious senescence, and may affect fertility and the overall individual well-being. Mitochondria play a central role in the maintenance of any cell health. Then mitochondrial dysfunctions may be responsible also for a negative impact on the quality, number, and function of oocytes, leading to different age-related reproductive disorders, impaired oogenesis, and embryogenesis. Although a large number of researches have shown clearly that mitochondrial dysfunction and morphology changes affect the maintenance and function of all major organs and tissues, such as the brain, heart, skeletal muscle, liver, and others the mechanisms contributing to early ovarian aging, a decrease of oocyte quality, and infertility remain unclear. In this review, we summarize the role of mitochondrial dysfunction in ovarian aging, presenting recent findings on morpho-functional changes in these organelles, and highlighting how their dysfunction accelerates ovary and cell senescence. We also explore their impact on oocyte functions. The reported data highlight the critical role of mitochondria in maintaining and enhancing oocyte quality, indicating that future studies should further focus on the mechanisms underlying mitochondrial damage and on identifying mitochondrial targets that may offer promising strategies to preserve, recover, and extend fertility in aging women.

Lindane, a persistent organochlorine pesticide, exerts toxic effects on the female reproductive system, compromising oocyte quality and maturation. However, the effects of this pesticide on mammalian oocyte morphology and ultrastructure remain unknown. This study investigated the effects of Lindane on mouse oocyte ultrastructure using an in vitro model with Transmission Electron Microscopy (TEM) at concentrations from 1 to 100 μM. The results revealed a progressive dose-related trend of alterations: at 1 μM, mild swelling of smooth endoplasmic reticulum (SER) vesicles; at 10 μM, increased SER dilation and cytoplasmic disorganization; and at 100 μM, pronounced vacuolization, mitochondrial swelling, dense lamellar bodies (dlbs), and multivesicular bodies (MVBs) indicative of autophagic activity. Mitochondrial alterations increased significantly with concentration: 3.2 ± 0.8 (control), 5.7 ± 1.0 (1 μM), 9.4 ± 1.5 (10 μM), and 16.8 ± 2.3 (100 μM) altered mitochondria per oocyte (p < 0.01). Vacuole frequency was notably elevated at 100 μM (4.3 ± 1.1 vs. 0.7 ± 0.5 in controls), and mislocalization of organelles within the ooplasm was observed. In conclusion, Lindane-induced oocyte ultrastructural alterations were observed at all tested concentrations but were more pronounced at 100 μM. These results highlight its impact on female fertility and may guide the search for protective agents, as well as efforts to reduce environmental exposure to endocrine disruptors.