Does aspirin-induced oxidative stress cause asthma exacerbation?

Abstract

Aspirin-induced asthma (AIA) is a distinct clinical syndrome characterized by severe asthma exacerbations after ingestion of aspirin or other non-steroidal anti-inflammatory drugs. The exact pathomechanism of AIA remains unknown, though ongoing research has shed some light. Recently, more and more attention has been focused on the role of aspirin in the induction of oxidative stress, especially in cancer cell systems. However, it has not excluded the similar action of aspirin in other inflammatory disorders such as asthma. Moreover, increased levels of 8-isoprostanes, reliable biomarkers of oxidative stress in expired breath condensate in steroid-naïve patients with AIA compared to AIA patients treated with steroids and healthy volunteers, has been observed. This review is an attempt to cover aspirin-induced oxidative stress action in AIA and to suggest a possible related pathomechanism.

Keywords: aspirin-induced asthma; free radicals; isoprostanes; nasal polyps.

Figure 1

Diagram of glutathione homeostasis

Figure 2

Chemical structures of ascertained isoprostanes

Figure 3

Apoptotic mechanism of aspirin action. According to the results, aspirin leads to inhibition of NFκB and next reduces Bcl2 protein expression. In turn, Bcl2 protein reduction causes TRAIL and TNF-α-induced apoptosis by activation of various caspases, conformational change and translocation of Bax and cytochrome c release. Another relative molecular mechanism of aspirin is abrogation of IL-6-IL6R-STAT3 signalling pathway that may also result in reduction of Bcl2 protein expression

Figure 4

Various aspirin actions in cell