Toxicological studies have identified polycyclic aromatic hydrocarbons (PAH) in human breast milk, smoked and barbequed food, although the largest contribution of PAH intake into the body are cereals and cereals products. The major effects attributable to PAH appeared to occur in the liver, lungs, the hematopoietic system, and the kidney. Nevertheless, more precise mechanisms by which PAH initiates its pathological features are not fully understood. In the present study, we evaluated levels of myeloperoxidase activity, its association with nitric oxide synthesis (NO), levels of uric acid (UA) in circulating blood and glucose in female rats exposed to environmental toxicants. A higher concentration of hydrogen peroxide activates myeloperoxidase, which acts as a leucocyte attractant, contributing to enhanced iNOS activity. In parallel, uric acid in addition to its pro-inflammatory effects aggravates insulin resistance and hyperglycemia, which worsens the process. Our findings suggest potential intermediate mechanisms involved in the inflammatory effects of PAH, which might give insight for the involvement of environmental toxicants not only in carcinogenesis but also in its association with acute cardiovascular disease and induction of multi-organ damage. The development of iNOS inhibitors might be beneficial in certain inflammatory disorders.
Keywords: Oxidative stress; PAH toxicant; liver; myeloperoxidase activity (MPO); nitric oxide (NO) synthesis.