The aryl hydrocarbon receptor (AhR) activation mediates benzo(a)pyrene-induced overexpression of AQP3 and Notch1 in HaCaT cells.

The aim of this study was twofold: (1) evaluate the effect of benzo[a]pyrene (BaP) on expression levels of AQP3 and Notch1 genes in HaCaT cells exposed "in vitro" and (2) investigate the possible biological role of assessed genes by bioinformatics methods. Cells were exposed to increasing concentrations of BaP (0.0-4.0 µM) for 1-4 days. After treatments, cell viability and expression levels of AhR, CYP1A1, AQP3, and Notch1 genes were evaluated. The possible biological role of assessed genes was evaluated using bioinformatics tools. Low cytotoxicity in HaCaT cells dosed with BaP was detected. A significant overexpression (p < .05) of CYP1A1, AQP3, and Notch1 was found in exposed HaCaT cells. The gene expression upregulation was dependent on AhR activation. The bioinformatics analysis showed that these genes were enriched in related cancer signaling pathways. The findings suggest that AQP3 and Notch1 are upregulated by AhR activation in HaCaT cells exposed to BaP.

Impact of arsenic exposure on clinical biomarkers indicative of cardiovascular disease risk in Mexican women.

An appropriate and precise identification of high-risk individuals to develop cardiovascular diseases (CVD) is of high importance to reduce these kinds of diseases, a major health concern worldwide. Therefore, the aim of this research was to evaluate prognostic CVD biomarkers in Mexican women exposed to inorganic arsenic via drinking water. Then, a cross-sectional study including 190 women was achieved. Urinary arsenic (UAs) levels were analyzed as exposure biomarker to that metalloid. While, plasma asymmetric dimethylarginine (ADMA), adipocyte fatty acid-binding protein (FABP4), adiponectin, and chemerin levels, hypertriglyceridemic waist (HW) phenotype, atherogenic index of plasma (AIP), and Framingham risk score (FRS) were assessed as prognostic CVD biomarkers. Mean UAs level detected in the evaluated urinary samples was 45.0 ±â€¯40.0 µg/g creatinine. In addition, mean plasma ADMA, FABP4, chemerin and adiponectin levels were 0.68 µmol/L, 20.3 ng/mL, 12.5 µg/mL, and 255 ng/mL, correspondingly. Approximately, 54% of women participants displayed an HW phenotype. Regarding AIP and FRS values, 0.12 ±â€¯0.15 and 7.50 ±â€¯8.00 were found, respectively. Besides, strong and significant associations (p < 0.05) between UAs and AIP, ADMA, and FABP4 were distinguished. Also, after a multivariate analysis, the association between those variables persisted after adjustment for traditional risk factors of CVD. In conclusion, according to the results found in this research, the most sensible CVD biomarkers distinguished in this study were AIP, ADMA, and FABP4. Nevertheless, more studies are necessary to confirm the results found in this investigation.

Influence on serum asymmetric dimethylarginine (ADMA) concentrations of human paraoxonase 1 polymorphism (Q192R) and exposure to polycyclic aromatic hydrocarbons (PAHs) in Mexican women, a gene-environment interaction.

It has been demonstrated that Cardiovascular Diseases (CVD) are a consequence of the combination of genetic and environmental factors and/or the interaction between them. Therefore, the aim of this study was to evaluate the impact of polycyclic aromatic hydrocarbon (PAHs) exposure and PON1 Q192R polymorphism (genetic susceptibility) on serum asymmetric dimethylarginine (ADMA) levels in Mexican women (n = 206). Urinary 1-hydroxypyrene concentrations (1-OHP; exposure biomarker for PAHs) were quantified using a high-performance liquid chromatography technique, PON1 Q192R polymorphism was genotyped using TaqMan probes and serum ADMA concentrations were evaluated using a commercially available ELISA kit. Urinary 1-OHP levels detected in this study ranged from 0.07 to 9.37 µmol/mol of creatinine (0.13-18.0 µg/g of creatinine). Regarding allele frequency (PON1 Q192R polymorphism), the 192Q-allele frequency was 0.43 and for the 192R-allele it was 0.57. In relation to serum ADMA levels, the levels ranged from 0.06 to 1.46 µmol/L. Moreover, multiple linear regression analysis was performed and associations between urinary 1-OHP levels (ß = 0.05, p = 0.002), PON1 Q192R polymorphism (ß = 0.04, p = 0.003) and serum ADMA concentrations were found. Besides, an interaction (gene-environment interaction) of both independent variables (1-OHP and PON1 polymorphism) on serum ADMA levels was found (ß = 0.04, p = 0.02) in the constructed multiple linear model. Therefore, according to the significance of this research, it is necessary to execute health programs to reduce cardiovascular risk in the assessed population.

Serum adipocyte-fatty acid binding protein (FABP4) levels in women from Mexico exposed to polycyclic aromatic hydrocarbons (PAHs).

Recent studies indicate that exposure to polycyclic aromatic hydrocarbons (PAHs) is a very important risk factor for the development of cardiovascular diseases (CVDs). Correspondingly, adipocyte-fatty acid binding protein (FABP4, also known as aP2 and AFABP) has been proposed as a new, meaningful and useful biomarker to predict metabolic and cardiovascular diseases. Therefore, the aim of this study was to evaluate serum FABP4 levels in Mexican women exposed to PAHs. Urinary 1-hydroxypyrene ((1-OHP), exposure biomarker for PAHs) levels were quantified using a high-performance liquid chromatography (HPLC) technique, and serum FABP4 concentrations were analyzed using a commercially available ELISA kit. The mean urinary 1-OHP level found in women participating in this study was 1.30 ± 1.10 µmol/mol creatinine (2.45 ± 2.10 µg/g creatinine). Regarding serum FABP4 concentrations, the levels ranged from 3.80 to 62.5 ng/mL in the assessed population. Moreover, a significant association (p < 0.001) was found between urinary 1-OHP levels and serum FABP4 concentrations in women after adjusting for potential confounding variables. The presented data in this study can be considered only as a starting point for further studies. Then, in order to elucidate whether FABP4 represents a risk factor for CVD disease in humans exposed to air contaminants (such as PAHs), large epidemiological studies are necessary.