Neural tube defects (NTDs) are malformations of the central nervous system that represent the second most common cause of congenital morbidity and mortality, following cardiovascular abnormalities. Maternal nutrition, particularly folic acid, a B vitamin, is crucial in the etiology of NTDs. FA plays a key role in DNA methylation, synthesis, and repair, acting as a cofactor in one-carbon transfer reactions essential for neural tube development. Randomized trials have shown that FA supplementation during preconceptional and periconceptional periods reduces the incidence of NTDs by nearly 80%. Consequently, it is recommended that all women of reproductive age take 400 µg of FA daily. Many countries have introduced FA fortification of staple foods to prevent NTDs, addressing the high rate of unplanned pregnancies. These policies have increased FA intake and decreased NTD incidence. Although the precise mechanisms by which FA protects against NTDs remain unclear, compelling evidence supports its efficacy in preventing most NTDs, leading to national recommendations for FA supplementation in women. This review focuses on preconceptional and periconceptional FA supplementation in the female population of the Visegrad Group countries (Slovakia, Czech Republic, Poland, and Hungary). Our findings emphasize the need for a comprehensive approach to NTDs, including FA supplementation programs, tailored counseling, and effective national-level policies.

This in vivo study performed in rat adjuvant arthritis aims to advance the understanding of astaxanthin’s therapeutic properties for the possible treatment of rheumatoid arthritis (RA) in monotherapy and along with the standard RA treatment, methotrexate (MTX), in combination therapy. The main goal was to elucidate astaxanthin’s full therapeutic potential, evaluate its dose dependency, and compare its effects in monotherapy with other carotenoids such as β-carotene and β-cryptoxanthin (KXAN). Moreover, potential differences in therapeutic activity caused by using different sources of astaxanthin, synthetic (ASYN) versus isolated from Blakeslea trispora (ASTAP), were evaluated using one-way ANOVA (Tukey-Kramer post hoc test). KXAN was the most effective in reducing plasma MMP-9 levels in monotherapy, significantly better than MTX, and in reducing hind paw swelling. The differences in the action of ASTAP and ASYN have been observed across various biometric, anti-inflammatory, and antioxidative parameters. In combined therapy with MTX, the ASYN + MTX combination proved to be better. These findings, especially the significant anti-arthritic effect of KXAN and ASYN + MTX, could be the basis for further preclinical studies.

We assessed lipid and lipoprotein profiles, along with oxidative stress (OS) parameters, in patients within the crucial 24 h period following an acute ischemic stroke (AIS), comparing those with and without coronary artery disease (CAD). We aimed to correlate these measures with clinical condition scales (NIHSS, mRS) post-AIS. This study included 27 AIS patients without CAD (AIS group) and 37 AIS patients with CAD (CAD-AIS group). Using polyacrylamide gel electrophoresis (Lipoprint system), we determined plasma LDL and HDL subfractions. Spectrophotometric methods were used to assess plasma antioxidant capacity, lipoperoxides, homocysteine (HC) levels, paraoxonase1, and catalase activities. We also measured urine isoprostanes and the activities of antioxidant enzymes (SOD, GPx) with commercial kits. CAD-AIS patients had notably higher HC levels, while there were no significant differences in lipoprotein subfractions and OS parameters between both groups. In the AIS group, mRS scores showed negative correlations with catalase, GPx activities, and total cholesterol. In the CAD-AIS group, atherogenic lipoproteins (IDLC, LDL2, LDL3–7) exhibited a significant positive correlation with mRS. This study underscores the role of dyslipidemia and OS in the development of AIS and CAD. It emphasizes the complex connections between specific biomarkers and post-stroke clinical outcomes. Our results suggest a significant impact of CAD treatment on lipid profile but not on homocysteine levels. The traditional narrative associating high cholesterol as the ultimate risk factor for cardiovascular diseases needs to be challenged, at least with respect to neurological outcomes. These insights may guide more targeted therapeutic approaches.

Background: Aging induces degenerative processes in the body, contributing to the onset of various age-associated diseases that affect the population. Inadequate dietary habits and low physical activity are major contributors to increased morbidity during aging. This study aimed to investigate the combined effects of omega-3 fatty acid supplementation and physical activity on the markers of oxidative stress and antioxidant defense mechanisms in aged male Wistar rats (23–24 months). Methods: The rats were randomly divided into four experimental groups: a sedentary control (placebo, no exercise), a trained (placebo and moderate-intensity graded aerobic exercise; Ex), and two trained groups supplemented with low (160 mg/kg of body weight; O1 + Ex) and high (320 mg/kg of body weight; O2 + Ex) doses of omega-3 fatty acids. The biochemical and functional parameters related to sarcopenia and the markers of oxidative stress were measured in blood and gastrocnemius muscle. Results: The results demonstrated dose-dependent, synergistic effects of omega-3 fatty acid supplementation and physical activity. The higher dose (320 mg/kg of body weight) improved plasma antioxidant capacity (TEAC, +21.01%, p < 0.01) and GPx activity (+78.05%, p < 0.05) while reducing CAT activity in erythrocytes (−19.92%, p < 0.05), likely as an adaptive stress response. Combined interventions also normalized cholesterol levels, improved the functional parameters of sarcopenia (stride length, +14.82%, p < 0.001), and enhanced antioxidant protection in aged rats. Conclusions: These findings highlight the potential of combining omega-3 fatty acid supplementation and physical activity to counteract aging-related degenerative changes. Further research is needed to elucidate the underlying mechanisms and evaluate the long-term benefits of these strategies in aging populations.

Microplastics (MPs) and nanoplastics (NPs) are widespread environmental contaminants with documented impacts on human health, particularly on the female reproductive system. Defined as polymeric fragments smaller than 5 mm, MPs (typically ranging from 1 µm to 5 mm) and NPs (smaller than 1 µm, often <100 nm) originate either from primary sources—intentionally manufactured for specific industrial applications—or from secondary sources through physical, chemical, or biological degradation of macroplastics. Human exposure occurs via multiple routes, including ingestion, inhalation, dermal absorption, and iatrogenic introduction, with growing evidence that these particles can accumulate in the ovaries, oocytes, and placental tissue. Experimental studies in rodents demonstrate that MPs and NPs induce oxidative stress, trigger inflammatory responses, and promote granulosa cell apoptosis, ultimately diminishing ovarian reserve and impairing folliculogenesis. Clinical and pilot human studies have confirmed the presence of MPs in placentas, umbilical cord blood, and meconium, indicating exposure from the earliest stages of development. Moreover, MPs and NPs may disrupt the hypothalamic–pituitary–ovarian axis, contributing to endocrine dysregulation and hormonal imbalance. Analytical methods such as Fourier-transform infrared spectroscopy, Raman spectroscopy, and scanning electron microscopy enable detection of these particles in biological samples, although methodological standardization remains insufficient. This paper summarizes current evidence on the exposure pathways, toxicological effects, and reproductive consequences of MPs and NPs in women. It further highlights existing research gaps and evaluates available analytical approaches to support future studies and develop strategies aimed at mitigating their detrimental impact on women’s reproductive health and fertility.

Syncytiotrophoblast (STB) vacuolization is common in term placentas, yet identical-appearing vacuoles are interpreted as physiological or degenerative depending on context, and, to our knowledge, a systematic description of their regional distribution within the STB in a defined cohort of uncomplicated term placentas is lacking. This pilot study aimed to define the regional organization of STB vacuolization in terminal villi within a single, consistently defined sampling site in uncomplicated term pregnancies. Using standardized transmission electron microscopy (TEM) protocols and blinded, independent scoring, we qualitatively evaluated vacuolar profiles in the subapical, perinuclear, and basal STB regions of placentas from ten uncomplicated singleton term pregnancies. Vacuolization followed a consistent, recurrent regional pattern across the cohort—small electron-lucent vesicles beneath the microvillous border, heterogeneous membrane-delimited compartments perinuclearly, and occasional larger vacuoles basally. These membrane-delimited profiles (membrane delimitation being an inclusion criterion) were observed in fields with preserved mitochondria and maintained microvillous architecture, suggesting that the regional context within the syncytial cytoplasm, rather than the mere presence of vacuoles, represents a candidate morphological criterion for distinguishing physiological vesicular activity from nonspecific degeneration, requiring direct validation against pathological comparator tissue. This pilot study is descriptive and requires validation in larger cohorts, pathological comparator groups, and complementary molecular approaches before its conclusions can be generalized; the proposed preliminary descriptive framework may offer a starting point for future studies interpreting trophoblast alterations in placental pathology and for contextualizing emerging environmental exposures, such as microplastic particles, at the maternal–fetal interface.