Concentrations of the pesticide DDT (dichlorodiphenyltrichloroethane) and its metabolite DDE (dichlorodiphenyldichloroethylene), in the blood of Mexican Americans, were evaluated to determine their relationships with diabetes and diabetic nephropathy. The data were derived from the National Health and Nutrition Examination Survey (NHANES) 1999–2004 (unweighted N = 1,411, population estimate = 13,760,609). The sample included teens, 12–19 years old, which accounted for 19.8% of the data. The time of the study overlapped the banning of DDT in Mexico in the year 2000, and those participants born in Mexico were exposed to DDT before they immigrated to the US. We sought to better understand the relationship of DDT with diabetes in a race/ethnicity group prone to develop diabetes and exposed to DDT. In this study, nephropathy was defined as urinary albumin to creatinine ratio >30 mg/g, representing microalbuminuria and macroalbuminuria, and total diabetes was defined as diagnosed and undiagnosed diabetes (glycohemoglobin, A1c ≥ 6.5%). The proportion with the isomer p,p′-DDT >0.086 ng/g (above the maximum limit of detection) was 13.3% for Mexican Americans born in the US, and 36.9% for those born in Mexico. Levels of p,p′-DDT >0.086 ng/g were associated with total diabetes with nephropathy (odds ratio = 4.42, 95% CI 2.23–8.76), and with total diabetes without nephropathy (odds ratio = 2.02, 95% CI 1.19–3.44). The third quartile of p,p′-DDE (2.99–7.67 ng/g) and the fourth quartile of p,p′-DDE (≥7.68 ng/g) were associated with diabetic nephropathy and had odds ratios of 5.32 (95% CI 1.05–26.87) and 14.95 (95% CI 2.96–75.48) compared to less than the median, respectively, whereas p,p′-DDE was not associated with total diabetes without nephropathy. The findings of this study differ from those of a prior investigation of the general adult US population in that there were more associations found with the Mexican Americans sample.

Perfluoroalkyl substances (PFASs) have been detected in organisms worldwide, including Polar Regions. The polar bear (Ursus maritimus), the top predator of Arctic marine ecosystems, accumulates high concentrations of PFASs, which may be harmful to their health. The aim of this study was to investigate which factors (habitat quality, season, year, diet, metabolic state [i.e. feeding/fasting], breeding status and age) predict PFAS concentrations in female polar bears captured on Svalbard (Norway). We analysed two perfluoroalkyl sulfonates (PFSAs: PFHxS and PFOS) and C8-C13 perfluoroalkyl carboxylates (PFCAs) in 112 plasma samples obtained in April and September 2012–2013. Nitrogen and carbon stable isotope ratios (δ15N, δ13C) in red blood cells and plasma, and fatty acid profiles in adipose tissue were used as proxies for diet. We determined habitat quality based on movement patterns, capture position and resource selection functions, which are models that predict the probability of use of a resource unit. Plasma urea to creatinine ratios were used as proxies for metabolic state (i.e. feeding or fasting state). Results were obtained from a conditional model averaging of 42 general linear mixed models. Diet was the most important predictor of PFAS concentrations. PFAS concentrations were positively related to trophic level and marine diet input. High PFAS concentrations in females feeding on the eastern part of Svalbard, where the habitat quality was higher than on the western coast, were likely related to diet and possibly to abiotic factors. Concentrations of PFSAs and C8-C10 PFCAs were higher in fasting than in feeding polar bears and PFOS was higher in females with cubs of the year than in solitary females. Our findings suggest that female polar bears that are exposed to the highest levels of PFAS are those 1) feeding on high trophic level sea ice-associated prey, 2) fasting and 3) with small cubs.

Chromium exposure from increasing industrial releases has become a threat for pregnant women due to the potential health effects on vulnerable embryos. Previous studies have suggested that maternal chromium exposure is associated with adverse birth outcomes, but no epidemiological research has been conducted to examine the relationship between chromium exposure and premature rupture of membranes (PROM). This study aimed at investigating the association of maternal urinary chromium exposure levels with PROM and was performed with 5408 pregnant women recruited from 2012 to 2014 in the city of Wuhan, China. Maternal urinary chromium collected before labor was adjusted with creatinine, and its association with PROM was evaluated using logistic regression. Each one unit increase in the natural logarithm transformed maternal urinary chromium concentration (μg/g creatinine), an odds ratio (OR) of 1.47 [95% confidence interval (CI): 1.36, 1.58] for PROM was observed. Compared to the lowest tertile of maternal urinary chromium, PROM was positively correlated with increased urinary levels of chromium (adjusted OR = 1.42; 95% CI: 1.09, 1.84 for the medium tertile; adjusted OR = 2.77; 95% CI: 2.18, 3.52 for the highest tertile). Additionally, the association of chromium with PROM appeared to be more significant among male infants (adjusted OR = 3.52; 95% CI: 2.51, 4.94 for the highest tertile) than female infants (adjusted OR = 2.16; 95% CI: 1.52, 3.06 for the highest tertile) (p for interaction = 0.05). Our large birth cohort showed an association between maternal urinary chromium levels and PROM, and the association may differ by infant gender. Further studies from different populations are needed to confirm the observed association.

In the present study, adult, healthy male Wistar rats (120 ± 10 g) were pre-treated by intragastric administration of cerium chloride (CeCl₃) 10 mg/kg (BW) each day during 60 days. Control animal were treated with omega 3, a polyunsaturated fatty acid (ω-3), by an intragastric administration at 10 mg/kg of BW for 60 days. Our results showed that CeCl₃-induced alterations in all tested oxidative stress markers. In fact, CeCl₃-induced the increase the level of both the creatinine concentration and the expression of lactate dehydrogenase, alkaline phosphatase, and transaminase activities in serum. On the other hand, CeCl₃ significantly increased the levels of lipid peroxidation in the renal and hepatic tissues. The capacity of CeCl₃ to generate reactive oxygen species (ROS) could explain his ability to induce morphological alterations, such as centrilobular hemorrhage, hepatic necrosis, and vacuolization of the cytoplasm in hepatic tissues, and the atrophy of the glomerulus and dilatation of urinary space in renal tissues. However, omega 3, after gastric administration, reduced significantly the toxic effect caused by CeCl₃ according to his high ability to scavenge ROS. The present study indicates that omega 3 is a significant compound with protective activity against intoxication with heavy metal, the cerium, and thus may be useful for chemoprevention.

Occupational exposure to low-level ionizing radiation (<1 Gy) was shown to enhance cell protection via attenuating an established inflammatory process. Nicotine, a major toxic component of cigarette smoke, is responsible for smoking-mediated renal dysfunction. The present study was therefore aimed to investigate the protective impact of ginger Zingiber officinale selenium nanoparticles (SeNPs) with whole-body low-dose gamma radiation (γ-R) against nicotine-induced nephrotoxicity in male albino rats. Nicotine intoxication was induced with 0.5 mg/kg BW. Rats received 0.1 mg SeNPs/kg BW by gastric gavage concomitant with 0.5 Gy γ-R over 4 weeks. Characterization studies showed the formation of spherical SeNPs with a size ranged from 10 to 30 nm in diameter with a thin film encapsulating the nanoballs. Our data revealed that nicotine induced renal dysfunction manifested by significant abnormal levels of kidney function markers (creatinine, urea, sodium and potassium) accompanied by increased levels of malondialdehyde along with a reduction in glutathione level, glutathione peroxidase, and glutathione S-transferase activities. It is worthy to note that nicotine toxicity induced significant increments in serum inflammatory markers: tumor necrosis factor-α and vascular cell adhesion protein 1. Western blotting showed marked significant elevation in caspase-3 activities against nicotine. The mRNA gene expression of inducible cyclooxygenase-2 gene was highly increased with nicotine intoxication while that of cyclooxygenase-1 did not show any changes. Interestingly, our data demonstrated that SeNPs in synergistic interaction with γ-R are efficacious control against nicotine-induced nephrotoxicity via anti-oxidant-mediated anti-inflammatory activities. Thus, it is tempting to recommend dietary approaches with ginger SeNPs for smokers at workplaces exposed occupationally and regularly to low-level ionizing radiation.

Aflatoxin is among the natural toxins that cause serious side effects on living things. Diosmin is also one of the compounds with broad pharmacological effects. In this study, the effects on the oxidant/antioxidant system of 50 mg/kg body weight/day dose of diosmin, aflatoxin (500 μg/kg body weight/day), and combined aflatoxin (500 μg/kg body weight/day) plus diosmin (50 mg/kg body weight/day) given to the stomach via catheter female adult Wistar Albino rats is examined. Forty rats were used in the experiment, and these animals were randomly allocated to four equal groups. The test phase lasted 21 days, and blood samples and tissue (liver and kidney) samples were taken after this period was over. Some biochemical parameters (glucose, triglyceride, cholesterol, blood urea nitrogen, creatinine, uric acid, lactate dehydrogenase, aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, total protein, albumin) and levels of malondialdehyde, nitric oxide, and 4-hydroxynonenal and activities of superoxide dismutase, catalase, and glutathione peroxidase were analyzed in the samples. The aflatoxin administered over the period indicated a significant increase in levels of malondialdehyde (MDA), nitric oxide (NO), and 4-hydroxynonenal (4-HNE) in all tissues and blood samples. Therewithal, the activity of antioxidant enzymes showed a change in the decreasing direction. Biochemical parameters of the group in which aflatoxin were administered alone changed unfavorably. Parallel effects were also observed in the histopathological findings of this group. The results showed that aflatoxin changed antioxidant/oxidant balance in favor of oxidant and eventually led to lipid peroxidation. Diosmin administration to aflatoxin-treated animals resulted in positive changes in antioxidant enzyme activities while the levels of MDA, NO, and 4-HNE were reduced in all tissues and blood samples examined. Diosmin alleviates the oxidative stress caused by aflatoxin. Similar improvement was observed in biochemical parameters of this group as well as in liver and kidney histopathology. No significant change was observed in the group treated with diosmin alone in terms of the parameters examined and histologic findings. As a result, diosmin may be included in compounds that can be used as a therapeutic and prophylactic agent in the event of the formation of aflatoxin exposure and poisoning in animals.

This study aims to determine the atmospheric concentrations of particulate matter 2.5 (PM₂.₅)-bounded polycyclic aromatic hydrocarbons (PAHs) and their association with their urinary metabolites in children and adolescents. This study was conducted from October 2014 to March 2016 in Isfahan, Iran. We measured 16 species of PAHs bounded to PM₂.₅ by gas chromatography mass spectrometry (GC/MS) from 7 parts of the city. Moreover, PAH urinary metabolites were measured in 186 children and adolescents, randomly selected from households. Urinary metabolites consisted of 1-hydroxy naphthalene (1-naphthol), 2-hydroxy naphthalene (2-naphthol), 9-hydroxy phenanthrene (9-phenanthrol), and 1-hydroxy pyrene using GC/MS. Considering the short half-lives of PAHs, we measured the metabolites twice with 4 to 6 months of time interval. We found that the ambient concentrations of PAHs were significantly associated with their urinary metabolites. 1-hydroxy naphthalene and 2-hydroxy naphthalene concentrations showed an increase of 1.049 (95% CI: 1.030, 1.069) and 1.047 (95% CI: 1.025, 1.066) for each unit increase (1 ng/m³) in ambient naphthalene. Similarly, 1-hydroxy pyrene showed an increase of 1.009 (95% CI: 1.006–1.011) for each unit increase (1 ng/m³) in ambient pyrene concentration after adjustment for body mass index, physical activity level, urinary creatinine, age, and sex. The association of urinary 9-hydroxyphenanthrene and ambient phenantherene was significant in the crude model; however after adjustment for the abovementioned covariates, it was no more significant. We found significant correlations between exposure to ambient PM₂.₅-bounded PAHs and their urinary excretion. Considering the adverse health effects of PAHs in the pediatric age group, biomonitoring of PAHs should be underscored; preventive measures need to be intensified.

The decline of cadmium pollution in fish farms is needed by any adequate method. The present study was designed to explore the effect of dietary cadmium contamination and its amelioration by using dietary clay, probiotic (Bactocell®), vitamin C, and vitamin E supplementation in Nile tilapia fish diet on growth rate, feed efficiency, blood components, and cadmium residues. Fish were separated into 15 groups, each group of fish was stocked into three aquaria and each contains 20 fishes. The fish of the first five groups were fed the basal diet, the second five groups were fed the basal diet contaminated with 25 mg cadmium/kg, and the third five groups were fed the same diet contaminated with 50 mg cadmium/kg. Within each dietary cadmium level, the first group was fed the diet without any supplementation, the second was fed the diet supplemented with natural clay (bentonite) at level 3%, the third group was fed the diet supplemented with 1 g Bactocell®/kg, the fourth group was fed the diet supplemented 50 mg vitamin E/kg, and the fifth group was fed the diet supplemented with 100 mg vitamin C/kg. Live body weight, daily body weight gain, and feed intake of Nile tilapia decreased significantly (P < 0.001) with increasing dietary cadmium level, while feed conversion was impaired. Fish group fed on diets contaminated with 50 mg cadmium/kg recorded the lowest live body weight and weight gain. Serum total protein and albumin concentration significantly (P < 0.001) decreased, while serum creatinine, AST, and ALT significantly (P < 0.001) increased with increasing cadmium level in fish diets. Blood hemoglobin and total erythrocyte (RBCs) significantly (P < 0.001 or 0.05) decreased with cadmium contamination in fish diets, while leukocytes were insignificantly affected. Body cadmium residues increased significantly (P < 0.001) by increasing cadmium level in fish diets. Live body weight, daily body weight gain, and feed intake of Nile tilapia increased significantly (P < 0.001) with feed additive supplementation in diets, also while feed conversion improved. Fish group fed on diets supplemented with probiotic Bactocell® or natural clay recorded higher body weight and gain rate than the other experimental groups. Serum total protein, blood hemoglobin, and total erythrocyte increased, while urea-N, creatinine, ALT, AST, and leukocytes decreased as affected with the feed additive supplementation. Feed additive supplementation in fish diets significantly (P < 0.001) decreased cadmium residues in fish bodies. Irrespective of dietary cadmium level, feed additive supplementation in fish diet improved the growth rate and decreased the concentrations of serum creatinine and ALT. The obtained results indicated that feed additive supplementation could modify the function of the kidney and liver in fish exposed to the cadmium toxicity.

This study investigated the ameliorative potential of exogenous phosphatidylcholine (PC) against aluminum-induced toxicity in male albino rats. Four groups of rats were used for this study (N = 8): group I served as the control, group II (PC treated) received L-α-phosphatidylcholine (egg yolk-derived) 100 mg/kg bwt/day orally, group III (aluminum treated) received aluminum chloride 100 mg/kg bwt/day orally, and group VI (aluminum + PC treated) received similar oral dose of aluminum and PC (100 mg/kg bwt/day). Treatment was continued for 8 weeks. Results revealed that aluminum chloride treatment leading to a significant elevation in serum aspartate aminotransferase, serum alanine aminotransferase, urea, creatinine, malondialdehyde, serum cytokines (tumor necrosis factor-α, interleukin-6), and brain content of acetylcholine, as well as a significant reduction in serum-reduced glutathione, serum testosterone, and brain content of acetylcholinesterase. Moreover, aluminum administration caused significant histopathological alteration in liver, kidney, brain, testes, and epididymis. Co-treatment with exogenous PC resulted in significant improvement in intensity of histopathologic lesions, serum parameters, testosterone level, proinflammatory cytokines, and oxidative/antioxidative status. However, it does not affect the brain content of acetylcholine and acetylcholinesterase. Conclusively, treatment with exogenous PC can retrieve the adverse effect of aluminum toxicities through its antioxidative and anti-inflammatory properties.

Recently, a great number of epidemiological studies have shown evidence that exposure to inorganic arsenic could have harmful effects on the cardiovascular system of humans. However, the underlying mechanisms through which arsenic induces cardiovascular toxic effects remain unclear. In this regard, epigenetic mechanisms have emerged as a probable connection between environment and disease phenotypes, including cardiovascular diseases. Therefore, this study aimed to evaluate epigenetic changes related to cardiotoxicity (miR-126 and miR-155 expression levels) in children from San Luis Potosi, Mexico exposed to inorganic arsenic. From 2014 to 2015, in a cross-sectional study, children (aged 6–12 years; n = 73) attending public schools at the studied sites were enrolled to take part in this study. Urinary arsenic was used as an exposure biomarker and analyzed by an atomic absorption spectrophotometry technique. On the other hand, miR-126 and miR-155 expression levels were evaluated by qRT-PCR. A mean urinary arsenic level of 30.5 ± 25.5 μg/g of creatinine was found. Moreover, the data showed a significant negative association (p < 0.05) between urinary arsenic concentrations and plasma miR-126 levels. However, an association between urinary arsenic concentrations and plasma miR-155 levels was not found (p > 0.05). In this regard, some investigations have shown an association between diminished plasma miR-126 levels and cardiovascular illnesses. The results found in this study are of concern. However, more similar studies including a larger sample size are necessary in order to clarify the real significance of the data.