peer reviewed | Previous studies described high concentrations of mercury (Hg) and selenium (Se) in the blood of harbour seals, Phoca vitulina from the North Sea. In the present study, we evaluated the in vitro potential protective effects of sodium selenite (Na2SeO3) and selenomethionine (SeMet) on cell proliferation of harbour seal lymphocytes exposed to MeHgCl 0.75 µM. In vitro exposure of ConA-stimulated T lymphocytes resulted in severe inhibition of DNA synthesis, likely linked to severe loss of mitochondrial membrane potential at 0.75 µM. Neither selenite nor SeMet showed a protective effect against MeHg toxicity expressed at the T lymphocyte proliferation level for harbour seals. Selenite and SeMet did not show negative effects regarding lymphocyte proliferation and mitochondrial membrane potential. To conclude, our results clearly demonstrated that MeHg affected in vitro immune cells exposure with no protective effects of selenium at a molar ratio Hg:Se of 1:10 in harbour seals from the North Sea.

Early interest in selenium by nutritionists was first identified in the 1930 s as a toxic element, nowadays it is known to be important in livestock and human diet. Its poisonous nature arouses the curiosity of researchers to investigate the impact of this element in human and animal metabolism. However, selenium has become the center of attention due to its physiological functions explained on the basis of its role as an active component of the enzyme glutathione peroxidase (GSH-PX), which is responsible for the animal antioxidant defense by destruction of hydrogen peroxide and lipid peroxides. Selenium metabolism and toxicity has been consistently studied in different species but data investigations on camelidae species are very limited. Our current study is configured to investigate the selenium intolerance in dromedary camel and carry out the symptoms related to continuous selenium supplementation. Investigations showed that camel is potentially sensitive to selenium excess. Several symptoms revealed by their different intensity from 3 batches, resumed in alopecia - abnormal movement and posture, breathing difficulties, prostration, diarrhea, lost of weight and nervous alteration. (Résumé d'auteur)

Cadmium (Cd) and lead (Pb) are known to enhance immune cell damages and to decrease cellular immunity, promoting higher susceptibility to infectious diseases. Selenium (Se) is an essential element involved in immunity and reactive oxygen species scavenging. This study aimed at evaluating how Cd and Pb and low nutritional (Se) quality modulate immune response to a bacterial lipopolysaccharide (LPS) challenge in wood mice (Apodemus sylvaticus). Mice were trapped near a former smelter in northern France in sites of High or Low contamination. Individuals were challenged immediately after capture or after five days of captivity, fed a standard or a Se-deficient diet. Immune response was measured with leukocyte count and plasma concentration of TNF-α, a pro-inflammatory cytokine. Faecal and plasma corticosterone (CORT), a stress-hormone involved in anti-inflammatory processes, was measured to assess potential endocrine mechanisms. Higher hepatic Se and lower faecal CORT were measured in free-ranging wood mice from High site. LPS-challenged individuals from High site showed steeper decrease of circulating leukocytes of all types, higher TNF-α concentrations, and a significant increase of CORT, compared to individuals from Low site. Challenged captive animals fed standard food exhibited similar patterns (decrease of leukocytes, increase of CORT, and detectable levels of TNF-α), with individuals from lowly contaminated site having higher immune responses than their counterparts from highly polluted site. Animals fed Se-deficient food exhibited lymphocytes decrease, no CORT variation, and average levels of TNF-α. These results suggest (i) a higher inflammatory response to immune challenge in free-ranging animals highly exposed to Cd and Pb, (ii) a faster recovery of inflammatory response in animals lowly exposed to pollution when fed standard food than more exposed individuals, and (iii) a functional role of Se in the inflammatory response. The role of Se and mechanisms underlying the relationship between glucocorticoid and cytokine remain to be elucidated.

Considerable investigations have been carried out to address the relationship between ambient fine particulate matter (PM₂.₅) and blood pressure (BP) in patients with hypertension. However, few studies have explored the influence of PM₂.₅ and its constituents on Trimethylamine N-oxide (TMAO), an established risk factor for hypertension and cardiovascular disease (CVD), particularly in severely air-polluted areas. To explore the potential impact of PM₂.₅ constituents on BP, plasma hormones, and TMAO, a panel study was conducted to investigate changes in BP, plasma hormones, and TMAO in response to ambient air pollution exposure in stage 1 hypertensive young adults. Linear mixed effect models were used to estimate the cumulative effects of fine particulate matters (PM₂.₅) and its constituents on BP, plasma hormones and TMAO. We found that one interquartile range (IQR) (35 μg/m³) increase in 0–1 day moving-average PM₂.₅ concentrations was statistically significantly associated with elevated systolic blood pressure (SBP), diastolic blood pressure (DBP), and mean arterial pressure (MAP) with estimated values of 0.13 (95% confidence interval (CI): 0.03 to 0.23) mmHg, 0.18 (95% CI: 0.08 to 0.28) mmHg, and 0.17 (95% CI: 0.09 to 0.26) mmHg, respectively. Hormone disturbance in the renin-angiotensin-aldosterone system was also associated with PM₂.₅ exposure. Elevated TMAO levels with an IQR increase for 0–4, 0–5, 0–6 moving-average concentrations of PM₂.₅ were found, and the increased values ranged from 26.28 (95% CI: 2.92 to 49.64) to 60.78 (31.95–89.61) ng/ml. More importantly, the PM₂.₅-bound metal constituents, such as manganese (Mn), titanium (Ti), and selenium (Se) showed robust associations with elevated BP and plasma TMAO levels. This study demonstrates associations between PM₂.₅ metal constituents and increased BP, changes in plasma hormones and TMAO, in stage 1 hypertensive young adults. Source control, aiming to reduce the emission of PM₂.₅-bound metals should be implemented to reduce the risk of hypertension and CVD.

The fetus is prenatally exposed to a mixture of organochlorine pesticides (OCPs), mercury (Hg), docosahexaenoic acid (DHA), eicosapentaenoic acid (EPA) and selenium (Se) through maternal seafood consumption in real-life scenario. Prenatal exposure to these contaminants and nutrients has been suggested to affect thyroid hormone (TH) status in newborns, but the potential relationships between them are unclear and the joint effects of the mixture are seldom analyzed. The aim of the study is to investigate the associations of prenatal exposure to a mixture of OCPs, Hg, DHA, EPA and Se with TH parameters in newborns. 228 mother-infant pairs in Shanghai, China were included. We measured 20 OCPs, total Hg, DHA, EPA and Se in cord blood samples as exposure variables. The total thyroxine (TT4), free thyroxine (FT4), total triiodothyronine (TT3), free triiodothyronine (FT3), and thyroid-stimulating hormone (TSH) levels and the FT3/FT4 ratio in cord serum were determined as outcomes. Using linear regression models, generalized additive models and Bayesian kernel machine regression, we found dose-response relationships of the mixture component with outcomes: among the contaminants, p,p'-DDE was the most important positive predictor of TT3, while HCB was predominantly positively associated with FT3 and the FT3/FT4 ratio, indicating different mechanisms underlying these relationships; among the nutrients, EPA was first found to be positively related to the FT3/FT4 ratio. Additionally, we found suggestive evidence of interactions between p,p'-DDE and HCB on both TT3 and FT3, and EPA by HCB interactions for TT3, FT3 and FT3/FT4 ratio. However, the overall effects of the mixture on thyroid hormone parameters were not significant. Our result suggests that prenatal exposure to p,p’-DDE, HCB and EPA as part of a mixture might affect thyroid function of newborns in independent and interactive ways. The potential biological mechanisms merit further investigation.

Lead is a metal that exists naturally in the Earth's crust and is a ubiquitous environmental contaminant. The alleviation of lead toxicity is important to keep human health under lead exposure. Biosynthesized selenium nanoparticle (SeNPs) and selenium-enriched Lactobacillus rhamnosus SHA113 (Se-LRS) were developed in this study, and their potentials in alleviating lead-induced injury to the liver and intestinal tract were evaluated in mice by oral administration for 4 weeks. As results, oral intake of lead acetate (150 mg/kg body weight per day) caused more than 50 times and 100 times lead accumulation in blood and the liver, respectively. Liver function was seriously damaged by the lead exposure, which is indicated as the significantly increased lipid accumulation in the liver, enhanced markers of liver function injury in serum, and occurrence of oxidative stress in liver tissues. Serious injury in intestinal tract was also found under lead exposure, as shown by the decrease of intestinal microbiota diversity and occurrence of oxidative stress. Except the lead content in blood and the liver were lowered by 52% and 58%, respectively, oral administration of Se-LRS protected all the other lead-induced injury markers to the normal level. By the comparison with the effects of normal L. rhamnosus SHA113 and the SeNPs isolated from Se-LRS, high protective effects of Se-LRS can be explained as the extremely high efficiency to promote lead excretion via feces by forming insoluble mixture. These findings illustrate the developed selenium-enriched L. rhamnosus can efficiently protect the liver and intestinal tract from injury by lead.

We aimed to explore the effects of mixtures of lead and various metals on blood pressure (BP) and the odds of pre-hypertension (systolic blood pressure (SBP) 120–139 mmHg, and/or diastolic blood pressure (DBP) 80–89 mmHg) and hypertension (SBP/DBP ≥140/90 mmHg) among Chinese adults in a cross-sectional study. This study included 11,037 adults aged 18 years or older from the 2017–2018 China National Human Biomonitoring. Average BP and 13 metals (lead, antimony, arsenic, cadmium, mercury, thallium, chromium, cobalt, molybdenum, manganese, nickel, selenium, and tin) in blood and urine were measured and lifestyle and demographic data were collected. Weighted multiple linear regressions were used to estimate associations of metals with BP in both single and multiple metal models. Weighted quantile sum (WQS) regression was performed to assess the relationship between metal mixture levels and BP. In the single metal model, after adjusting for potential confounding factors, the blood lead levels in the highest quartile were associated with the greater odds of both pre-hypertension (odds ratio (OR): 1.56, 95% CI: 1.22–1.99) and hypertension (OR:1.75, 95% CI: 1.28–2.40) when compared with the lowest quartile. We also found that blood arsenic levels were associated with increased odds of pre-hypertension (OR:1.31, 95% CI:1.00–1.74), while urinary molybdenum levels were associated with lower odds of hypertension (OR:0.68, 95% CI:0.50–0.93). No significant associations were found for the other 10 metals. WQS regression analysis showed that metal mixture levels in blood were significantly associated with higher SBP (β = 1.56, P < 0.05) and DBP (β = 1.56, P < 0.05), with the largest contributor being lead (49.9% and 66.8%, respectively). The finding suggests that exposure to mixtures of metals as measured in blood were positively associated with BP, and that lead exposure may play a critical role in hypertension development.

Bacteria play crucial roles in the biogeochemical cycle of arsenic (As) and selenium (Se) as these elements are metabolized via detoxification, energy generation (anaerobic respiration) and biosynthesis (e.g. selenocysteine) strategies. To date, arsenic and selenium biomineralization in bacteria were studied separately. In this study, the anaerobic metabolism of As and Se in Shewanella sp. O23S was investigated separately and mixed, with an emphasis put on the biomineralization products of this process. Multiple analytical techniques including ICP-MS, TEM-EDS, XRD, Micro-Raman, spectrophotometry and surface charge (zeta potential) were employed. Shewanella sp. O23S is capable of reducing selenate (SeO₄²⁻) and selenite (SeO₃²⁻) to red Se(-S)⁰, and arsenate (AsO₄³⁻) to arsenite (AsO₃³⁻). The release of H₂S from cysteine led to the precipitation of AsS minerals: nanorod AsS and granular As₂S₃. When As and Se oxyanions were mixed, both As–S and Se(-S)⁰ biominerals were synthesized. All biominerals were extracellular, amorphous and presented a negative surface charge (−24 to −38 mV). Kinetic analysis indicated the following reduction yields: SeO₃²⁻ (90%), AsO₄³⁻ (60%), and SeO₄²⁻ (<10%). The mix of SeO₃²⁻ with AsO₄³⁻ led to a decrease in As removal to 30%, while Se reduction yield was unaffected (88%). Interestingly, SeO₄²⁻ incubated with AsO₄³⁻ boosted the Se removal (71%). The exclusive extracellular formation of As and Se biominerals might indicate an extracellular respiratory process characteristic of various Shewanella species and strains. This is the first study documenting a complex interplay between As and Se oxyanions: selenite decreased arsenate reduction, whereas arsenate stimulated selenate reduction. Further investigation needs to clarify whether Shewanella sp. O23S employs multi-substrate respiratory enzymes or separate, high affinity enzymes for As and Se oxyanion respiration.

The largest and most variable step of selenium (Se) assimilation into aquatic ecosystems is the rapid uptake of aqueous Se by primary producers. These organisms can transfer more harmful forms of Se to higher trophic levels via dietary pathways, although much uncertainty remains around this step of Se assimilation due to site-specific differences in water chemistry, hydrological and biogeochemical characteristics, and community composition. Thus, predictions of Se accumulation are difficult, and boreal lake systems are relatively understudied. To address these knowledge gaps, five static-renewal field experiments were performed to examine the bioaccumulation of low, environmentally relevant concentrations of Se, as selenite, by naturally grown periphyton from multiple boreal lakes. Periphyton rapidly accumulated Se at low aqueous Se concentrations, with tissue Se concentrations ranging from 8.0 to 24.9 μg/g dry mass (dm) in the 1–2 μg Se/L treatments. Enrichment functions ranged from 2870 to 12 536 L/kg dm in the 4 μg Se/L treatment, to 11 867–22 653 L/kg dm in the 0.5 μg Se/L treatment among lakes. Periphyton Se uptake differed among the five study lakes, with periphyton from mesotrophic lakes generally accumulating more Se than periphyton from oligotrophic lakes. Higher proportions of charophytes and greater dissolved inorganic carbon in more oligotrophic lakes corresponded to less periphyton Se uptake. Conversely, increased proportions of bacillariophytes and total dissolved phosphorus in more mesotrophic lakes corresponded to greater periphyton Se uptake. Periphyton community composition and water chemistry variables were correlated, limiting interpretation of differences in periphyton Se accumulation among lakes. The results of this research provide insight on the biodynamics of Se assimilation at the base of boreal lake food webs at environmentally relevant concentrations, which can potentially inform ecological risk assessments in boreal lake ecosystems in North America.