Combustion products of 1,3-butadiene inhibit catalase activity and induce expression of oxidative DNA damage repair enzymes in human bronchial epithelial cells

Abstract

1,3-Butadiene, an important petrochemical, is commonly burned off when excess amounts need to be destroyed. This combustion process produces butadiene soot (BDS), which is composed of a complex mixture of polyaromatic hydrocarbons in particulates ranging in size from <1μm to 1 mm. An organic extract of BDS is both cytotoxic and genotoxic to normal human bronchial epithelial (NHBE) cells. Based on the oxidizing potential of BDS, we hypothesized that an organic extract of this particulate matter would: 1) cause enzyme inactivation due to protein amino acid oxidation; and 2) induce oxidative DNA damage in NHBE cells. Thus, our aims were to determine the effect of butadiene soot ethanol extract (BSEE) on both enzyme activity and expression of proteins involved in the repair of oxidative DNA damage. Catalase was found to be sensitive to BDS as catalase activity was potently diminished in the presence of BSEE. Using Western analysis, both the alpha isoform of human 8-oxoguanine DNA glycosylase (α-hOGG1) and human apurinic/apyrimidinic endonuclease (APE-1) were shown to be significantly overexpressed as compared to untreated controls after exposure of NHBE cells to BSEE. Our results indicate that BSEE is capable of effectively inactivating the antioxidant enzyme catalase, presumably via oxidation of protein amino acids. The presence of oxidized proteins may partially explain the extranuclear fluorescence that is detected when NHBE cells are treated with an organic extract of BDS. Overexpression of both α-hOGG1 and APE-1 proteins following treatment of NHBE cells with BSEE suggests that this mixture causes oxidative DNA damage.

Age specific responses to acute inhalation of diffusion flame soot particles: Cellular injury and the airway antioxidant response

“…In agreement with our protein expression findings, catalase has been shown to increase in activity with postnatal maturation in the rat lung (Chen and Frank, 1993). Interestingly, exposure of normal human bronchial epithelial cells to butadiene soot, as well as exposure of adult rats to diesel exhaust particles, has been shown to significantly decrease catalase enzyme activity (Kennedy et al, 2009; Rengasamy et al, 2003). Reduction of catalase activity in the rats was thought to be related to the carbonaceous core of the diesel exhaust, a feature that is well preserved in our DFP exposure particles (Rengasamy et al, 2003).…”

Association of volatile organic compound exposure with metabolic syndrome and its components: a nationwide cross-sectional study

“…McGraw et al found exposure to BD metabolites was significantly linked to elevated SBP and endothelial dysfunction, and DHBMA was one of the most important metabolites of the group in relation to SBP and DBP, as indicated by a higher posterior inclusion probability in the Bayesian kernel machine regression model [ 41 ]. Previous experimental studies also revealed that BD exposure may trigger oxidative stress, induce the elevation of reactive oxygen species, and activate the mitochondrial apoptotic pathway [ 42 , 43 ]. Similarly, several epidemiological studies further found positive associations of BD exposure with increased oxidative stress markers, vascular endothelial dysfunction, and several cardiovascular risk factors among the young population in China [ 40 , 44 , 45 ].…”

Measuring 1, 3-Butadiene and Simulation of its Releasing Method by GIS Application and Cancer Risk Assessment in Tehran in 2019-2020

“…Some factors such as cigarette smoke and other toxicants (i.e., benzene and styrene) may confound the true chronic effects caused by 1, 3-Butadiene exposure [6]. However, 1, 3-Butadiene is a carcinogenic agent, which was reported to cause Deoxyribonucleic Acid (DNA) damage [7,8]. This toxicant metabolically activates the genotoxic epoxides, resulting in abnormality in DNA adducts and chromosomes [9].…”