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Alpha-glucosidase (GAA) activity can be affected by exogenous substances. Hydroxylated polycyclic aromatic hydrocarbons (OH-PAHs) are typical metabolites of PAHs that can enter the body through various routes. The effects of 1-hydroxynaphthalene (1-OHNap) and 1-hydroxypyrene (1-OHPyr) on GAA activity and the potential mechanisms were investigated viamultispectroscopic methods and molecular docking. First-order derivative synchronous spectrofluorimetry was successfully applied to analyze the fluorescence quenching of GAA in the GAA-1-OHNap and GAA-1-OHPyr systems. 1-OHNap and 1-OHPyr had strong inhibitory effects on GAA activity. GAA could bind with 1-OHNap and 1-OHPyr in 1:1 mode with binding constants of 3.97 × 104 and 9.42 × 104 L/mol at 298 K. Hydrophobic interactions and hydrogen bonds played pivotal roles in the interactions. 1-OHNap was located closer to the active site of GAA than 1-OHPyr. This work suggests that the disturbance of glycometabolism by exogenous pollutants in the human body is worthy of attention and further investigation.

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RESUMEN

Hydroxylated polycyclic aromatic hydrocarbons (OH-PAHs) can bind with functional biomacromolecules and thus cause toxic effects in vivo. Four types of cyclodextrins (CDs) were selected to explore their potential ability to regulate the bindings between 1-hydroxypyrene (1-OHPyr) and bovine serum albumin (BSA) using multi-spectroscopic methods combined with molecular docking. The results showed that the four CDs caused varied modulating effects on the binding of BSA with 1-OHPyr, and the effects of γ-CD and (2-hydroxypropyl)-ß-CD (HPCD) are the most significant. Specifically, γ-CD and HPCD could significantly reduce the binding affinity between 1-OHPyr and BSA, inhibit the micro-environmental changes of tryptophan residues, and slightly recover the helicity of BSA. The interactions and inclusion behavior of CDs with 1-OHPyr was the main reason why CDs could affect the binding of 1-OHPyr to BSA. The results indicated that γ-CD and HPCD might have potential application value in regulating the toxic effects of OH-PAHs.

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To reveal the potential effects of hydroxylated polycyclic aromatic hydrocarbons (OH-PAHs) on catalase (CAT), the interactions of 1-hydroxynaphthalene (1-OHNap), 9-hydroxyphenanthrene (9-OHPhe) and 1-hydroxypyrene (1-OHPyr) with CAT were investigated using multi-spectroscopic and molecular docking techniques. Fluorescence analysis showed that 1-OHNap, 9-OHPhe and 1-OHPyr can form 1:1 complex with CAT, with the binding constant of 6.31 × 103, 1.03 × 104 and 2.96 × 105 L mol-1 at 17 °C. Thermodynamic and docking parameters demonstrated that van der Waals' force, hydrogen bonds and hydrophobic interactions dominated the three binding processes. Molecular docking also revealed the specific binding mode of OH-PAHs with CAT. Synchronous fluorescence and circular dichroism spectral results indicated that the three OH-PAHs induced varied structural changes of CAT. Furthermore, CAT activity was promoted by 9-OHPhe, but inhibited by either 1-OHNap or 1-OHPyr. Under the maximum experimental concentration of OH-PAHs, the percent change of CAT activity induced by 1-OHNap, 9-OHPhe and 1-OHPyr were 8.42%, 4.26% and 13.21%.

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To explore whether the alteration of lncRNA expression is correlated with polycyclic aromatic hydrocarbons (PAHs) exposure and DNA damage, we examined PAHs external and internal exposure, DNA damage and lncRNAs (HOTAIR, MALAT1, TUG1 and GAS5) expression in peripheral blood lymphocytes (PBLCs) of 150 male coke oven workers and 60 non-PAHs exposure workers. We found the expression of HOTAIR, MALAT1, and TUG1 were enhanced in PBLCs of coke oven workers and positively correlated with the levels of external PAHs exposure (adjusted Ptrend < 0.001 for HOTAIR and MALAT1, adjusted Ptrend = 0.006 for TUG1). However, only HOTAIR and MALAT1 were significantly associated with the level of internal PAHs exposure (urinary 1-hydroxypyrene) with adjusted ß = 0.298, P = 0.024 for HOTAIR and ß = 0.090, P = 0.034 for MALAT1. In addition, the degree of DNA damage was positively associated with MALAT1 and HOTAIR expression in PBLCs of all subjects (adjusted ß = 0.024, P = 0.002 for HOTAIR and ß = 0.007, P = 0.003 for MALAT1). Moreover, we revealed that the global histone 3 lysine 27 trimethylation (H3K27me3) modification was positively associated with the degree of genetic damage (ß = 0.061, P < 0.001) and the increase of HOTAIR expression (ß = 0.385, P = 0.018). Taken together, our findings suggest that altered HOTAIR and MALAT1 expression might be involved in response to PAHs-induced DNA damage.