Tobacco-Smoke-Inducible Human Heme Oxygenase-1 Gene Expression

Abstract

Expression of stress-related genes are particularly induced following exposure to thiol-reactive compounds (Heikkila et al., 1982), reactive oxygen intermediates (ROI) (Keyse et al., 1989a, Keyse 1989b, Keyse 1990) (Alam et al., 1994), heavy metal cations (Alam et al., 1994; Takeda et al., 1994; kimberly et al., 1998), UV radiation (Lautier et al., 1992; Vile et al., 1994) and other chemical initiators of cellular stress responses such as lipopolysaccharides or hydrogen peroxide (H2O2) (Kurata et al., 1996; Camhi et al., 1995). These stimuli all induce the expression of a 32–34kDa protein identified as the microsomal, inducible, heme oxygenase-1 (HO-1), whose regulation is related to heat shock proteins (HSP) in rodents, but not in humans (Shibahara et al., 1985; Mitani et al., 1991; Clerget et al., 1990; Pizursky et al., 1990); a review showed (Stocker et al., 1990) that bile pigments produced by heme degradation catalyzed by HO-1 can function as anti-oxidants, while Keyse and Tyrrell (1989a) demonstrated that HO-1 is involved in the general cellular defence mechanisms against oxidative injury.