Smoking is the most important cause of morbidity and mortality in the world. In this context, smoking is the more relevant environmental factor involved in the genesis of articular diseases, such as rheumatoid arthritis (RA) and osteoarthritis (OA), but the mechanisms and cigarette compounds involved still unclear. Hydroquinone (HQ) is the most abundant pro-oxidative compound in cigarette smoke, as well as the metabolite of benzene biotransformation, which is also present in higher concentrations in cigarette smoke. Our previous data show that HQ exposure contributes to the development and worsening of RA by the collagen-induced arthritis model (AIC) in rats, revealing mechanisms not yet described for this xenobiotic. Non-combustible cigarettes have been proposed as alternatives in order to reduce damage caused to the smoking population, but studies regarding their toxicity are still inconclusive. These include tobacco products that heat but not burn (such as iQOS aerosol generated by the tobacco vapor), thus generating lower amounts of toxic constituents than cigarette smoke. Thus, we intend to investigate the mechanisms of HQ toxicity in both RA and OA diseases, and to investigate the iQOS aerosol toxicity in articular diseases, being the first in Brazil and one of the first in the world to investigate the later. Therefore, the studies will be conducted in experimental animals, and in samples obtained from smoking and non-smoking patients at the FCF / USP and at the University of Surrey, UK.
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