Evidence concerning effects of ambient air pollution on homocysteine (HCY) metabolism is scarce. We aimed to explore the associations between ambient particulate matter (PM) exposure and the HCY metabolism markers and to evaluate effect modifications by folate, vitamin B₁₂, and methylenetetrahyfrofolate reductase (MTHFR) C677T gene polymorphism. Between December 1, 2017 and January 5, 2018, we conducted a panel study in 88 young college students in Guangzhou, China, and received 5 rounds of health examinations. Real-time concentrations of PMs with aerodynamic diameter ≤2.5 (PM₂.₅), ≤1.0 (PM₁.₀), and ≤0.1 (PM₀.₁) were monitored, and the serum HCY metabolism markers (i.e., HCY, S-Adenosylhomocysteine [SAH], and S-Adenosylmethionine [SAM]) were repeatedly measured. We applied linear mixed effect models combined with a distributed lag model to evaluate the associations of PMs with the HCY metabolism markers. We also explored effect modifications of folate, vitamin B₁₂, and the MTHFR C677T polymorphism on the associations. We observed that higher concentrations of PM₂.₅ and PM₁.₀ were associated with higher serum levels of HCY, SAH, SAM, and SAM/SAH ratio (e.g., a 10 μg/m³ increase in PM₂.₅ during lag 0 day and lag 5 day was significantly associated with 1.3–19.4%, 1.3–28.2%, 6.2–64.4%, and 4.8–28.2% increase in HCY, SAH, SAM, and SAM/SAH ratio, respectively). In addition, we observed that the associations of PM₂.₅ with the HCY metabolism markers were stronger in participants with lower B vitamins levels. This study demonstrated that short-term exposure to PM₂.₅ and PM₁.₀ was deleteriously associated with the HCY metabolism markers, especially in people with lower B vitamins levels.

A multibiomarker approach was developed to evaluate the juvenile European flounder responses to a complex mixture of 9 polycyclic aromatic hydrocarbons (PAHs) and 12 polychlorinated biphenyls (PCBs). Exposure was performed through contaminated food pellets displaying: (1) PAH and PCB levels similar to those detected in the heavily polluted Seine estuary, respectively in sediments and in flatfish and (2) ten times these concentrations. Several biomarkers of the immune system (e.g., lysozyme concentration and gene expression of complement component C3 and TNF-receptor), DNA damage (e.g., Comet assay), energetic metabolism (e.g., activity of cytochrome C oxidase), detoxification process (e.g., cytochrome P450 1A1 expression level: CYP1A1; betaine homocysteine methyl transferase expression level: BHMT) were investigated after 14 and 29 days of contamination, followed by a 14-days recovery period. After 29 days of contamination, the detoxification activity (CYP1A1 expression level) was positively correlated with DNA damages; the increase of the BHMT expression level could also be related to the detoxification process. Furthermore, after the recovery period, some biomarkers were still upregulated (i.e., CYP1A1 and BHMT expression levels). The immune system was significantly modulated by the chemical stress at the two concentration levels, and the lysozyme appeared to be the most sensitive marker of the mixture impact.

Nutritional status could affect arsenic metabolism and toxicity in the general population chronically exposed to low levels of inorganic arsenic. In this study, we examined the association of serum folate and cobalamin with urinary concentrations of dimethylarsinic acid (DMA), the most abundant metabolite of inorganic arsenic measured in urine, in children and adults who participated in the 2003–2006 US National Health and Nutrition Examination Surveys. A total of 1161 children (aged 6–19 years) and 1938 adults (aged 20–85 years) were analyzed for the association using multivariate general linear models, adjusting for potential confounders. We observed a positive association between serum levels of folate and cobalamin and creatinine-corrected urinary concentrations of DMA in both children and adults. Furthermore, serum levels of folate and cobalamin were inversely associated with homocysteine (Hcy). These results suggest that dietary intake of folate and cobalamin may exhibit protective functions against arsenic toxicity by increasing arsenic metabolism to the less toxic metabolite DMA and decreasing serum levels of Hcy.

Lipid peroxidation and ROS generation are the pathogenesis of chronic fluoride toxicity, and its detrimental effects on human reproduction are noted drastically. The aim of the present study was to elucidate the defensive effects of soy protein concentrate (SPC) against sodium fluoride (NaF)-induced uterine dysfunction at biochemical and histological level. Rats were randomly distributed into four groups as control, NaF-treated (200 ppm), and SPC co-administered groups (20 mg and 40 mg/ 100 g body weight) for 16 days. SPC reversed the toxic effects of NaF. SPC significantly ameliorated the NaF-induced alterations of the antioxidant system in the uterus by decreasing lipid peroxidation products and by increasing antioxidant activities. SPC significantly counteracted the adverse effects of NaF on serum level of lactate dehydrogenase (LDH) and inflammatory markers Interleukin-6 (IL-6), tumor necrosis factor alpha (TNF-α) and nuclear factor kappa-B (NF-κB). Our results also explored that lipid profile was meaningfully altered due to NaF and also focused a diminution of circulating homocysteine (Hcy) and altered lipid profiles along with a diminished quantity of serum B₁₂ and B₉. However, both the doses of SPC reverted back serum levels of B₁₂, B₉, and Hcy status in similar fashion along with its corrective action on lipid profile. NaF-treated group exhibited a marked degree of reduction in the weights of ovary and uterus with an alteration of normal tissue histology and significant diminution in serum estradiol (ES) levels without fluctuating uterine estradiol receptor-α (ER-α). However, SPC restored the normal tissue histoarchitecture and also increased the functional efficiency and expression of the ER-α receptor by overturning the ES levels in NaF-treated rats. Moreover, both the doses of SPC were effective against NaF-induced alterations, although 40 mg SPC/100 g body weight had better efficacy in ameliorating the NaF-induced adverse effects on the uterus and ovary.

Physiological and genetic responses of age 0+ Platichthys flesus were investigated in the eutrophicated and moderately contaminated Vilaine estuary, during a 6-month survey. The main objective of this study was to explore the biological responses of fishes during their juvenile period in an estuarine system in order to detect a possible selective pressure induced by the environmental stress. Our results showed a general convergence in physiological responses along the survey: an increase in genotoxicity was associated with an increase in mRNA expression of ATPase and betaine homocysteine methyltransferase. These results could suggest an increase of cellular damage, energetic request, and detoxification rate related to the growing exposure time to stress. Considering the aging of the cohort, the genetic characteristics of the Vilaine flounder cohort came closer to the one observed in a highly stressed system, the Seine estuary, suggesting a potential selective pressure mainly induced by the chemical stress.