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© 2021 American Chemical Society.To provide insights into the cause of e–cigarette (e–cig) associated lung injury, we examined the effects of propylene glycol (PG) and glycerol (G), two common solvent carriers used to deliver nicotine/flavor, on markers of oxidative stress and inflammation in female B6C3F1 mice which had been used successfully in tobacco smoke (TS)–induced lung carcinogenesis. Mice exposed to air and TS were used as negative and positive controls, respectively. Using LC–MS/MS, we showed that PG/G alone, in the absence of nicotine, significantly increased the levels of 8–hydroxy–2′–deoxyguanosine (8–OHdG or its tautomer 8–oxodG), a biomarker of DNA oxidative damage, in lung and plasma of mice; moreover, addition of nicotine (12 and 24 mg/mL) in e–cig liquid appears to suppress the levels of 8–oxodG. Exposure to e–cig aerosols or TS induced nonsignificant increases of plasma C–reactive protein (CRP), a biomarker of inflammation; nonetheless, the levels of fibronectin (FN), a biomarker of tissue injury, were significantly increased by e–cig aerosols or TS. Although preliminary, our data showed that exposure to e–cig aerosols induced a higher score of lung injury than did control air or TS exposure. Our results indicate that the B6C3F1 mouse model may be suitable for an in–depth examination of the impact of e–cig on lung injury associated with oxidative stress and inflammation and this study adds to the growing evidence that the use of e–cig can lead to lung damage.
