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Carbonyl Toxification Hypothesis of Biological Aging
Published in Alvaro Macieira-Coelho, Molecular Basis of Aging, 2017
α,β-Unsaturated carbonyls have also been found in many other biological interactions, such as the base-propenals, which are oxidation products of sugars attached to DNA bases; acrolein and crotonaldehyde, which are air pollutants; and trans, trans-muconaldehyde, which is a microsomal metabolite of benzene.68 Pyruvaldehyde, also named methylglyoxal (MG), is another example of a cytotoxic and genotoxic DMcarbonyl. MG exists widely in food and beverages69 and may be produced during Maillard reactions.38 In biological systems, however, MG may also be synthesized by several metabolic pathways. For example, MG is synthesized from dihydroxylacetone phosphate when catalyzed by MG synthetase; MG may also be made from aminoacetone during the catabolism of L-threonine.70,71 On the other hand, MG may be eliminated by several biological pathways, including (1) conversion into D-lactate by the glutathione-requiring glyoxalase system, and (2) oxidation to pyruvate catalyzed by MG dehydrogenases.70 Although the functions of MG and its conversion to lactic acid by glyoxalase in biological system are still unclear, the glyoxalase system was found to be clearly related to DNA synthesis and cell proliferation, which may provide insights into cellular senescence.70
Crotonaldehyde exposure induces liver dysfunction and mitochondrial energy metabolism disorder in rats
Published in Toxicology Mechanisms and Methods, 2021
Shuman Zhang, Biao Zhang, Qi Zhang, Zhihu Zhang
Crotonaldehyde (C4H6O), a highly active α,β-unsaturated aldehyde, is widely used in food, beverage, tobacco, pesticide, cosmetic, dye, and rubber industries (Jha and Kumar 2006). Human exposure to crotonaldehyde is via both man-made and natural sources. Crotonaldehyde exists primarily in automobile exhaust, and wood and tobacco smoke. Meat, fish, fruits, and vegetables, however, also contain various levels of crotonaldehyde (Budiawan and Eder 2000). Crotonaldehyde is a highly toxic irritant that can cause damage to the respiratory tract, eyes, and skin. The U.S. Environmental Protection Agency has classified crotonaldehyde as a group C chemical substance (possible human carcinogen). Crotonaldehyde exposure can induce hepatotoxicity, precancerous lesions, or the formation of neoplastic nodules in rats (Chung et al. 1986). However, the mechanism underlying liver damage caused by crotonaldehyde exposure remains unclear. Liver provides energy for numerous physiological processes including immune system support, endocrine control of growth signaling pathways, metabolism, and decomposition of foreign compounds and drugs (Trefts et al. 2017). Liver cells have an abundance of mitochondria, sites of energy production that play an important role in regulating energy metabolism, signaling pathways, and apoptosis (Galluzzi et al. 2012). Therefore, exogenous poison exposure resulting in mitochondrial dysfunction is an important cause of liver injury (Binukumar et al. 2010; Serviddio et al. 2011).
Crotonaldehyde-induced alterations in testicular enzyme function and hormone levels, and apoptosis in the testes of male Wistar rats are associated with oxidative damage
Published in Toxicology Mechanisms and Methods, 2020
Biao Zhang, Ping Wei, Jinlong Men, Shuman Zhang, Hua Shao, Zhihu Zhang
Crotonaldehyde is a highly reactive α, β-unsaturated aldehyde, and is released into the atmosphere from several smoke sources such as cigarettes and automotive exhaust. It is also generated from physiological processes such as the metabolism of lipids and carcinogens (N-nitrosopyrrolidine and 1,3-butadiene). In vitro and in vivo studies have shown that crotonaldehyde exerts a broad spectrum of toxic effects. After oral administration to rats, it induced caspase-dependent apoptosis in BEAS-2B cells by reducing intracellular glutathione levels and elevating ROS levels in a dose-dependent manner, resulting in oxidative stress, which altered liver cell foci and caused neoplastic nodule formation and hepatocellular carcinoma (Salmon 1995; Ryu et al. 2013; Liu et al. 2010). Crotonaldehyde has been listed as one of nine constituents recommended for disclosure and monitoring by the World Health Organization (WHO) study group on tobacco product regulation (Haussmann 2012). Due to its extreme toxicity and ubiquity in different smoke sources, research is focused on its role in lung toxicity. However, the mechanisms of its toxic effects on reproductive organs are not well understood. Therefore, this study focused on crotonaldehyde-induced toxicity in reproductive organs after long-term exposure to low doses, to comprehend how its effects are stimulated in daily life exposure.
Long-term exposure to crotonaldehyde causes heart and kidney dysfunction through induction of inflammatory and oxidative damage in male Wistar rats
Published in Toxicology Mechanisms and Methods, 2019
Biao Zhang, Shuangshuang Li, Jinlong Men, Cheng Peng, Hua Shao, Zhihu Zhang
Crotonaldehyde (CAS No. 4170-30-3, C4H6O) is a highly reactive α,β-unsaturated aldehyde, which is used as an important intermediate to manufacture sorbic acid, dyes, pesticides, pharmaceuticals, and rubber antioxidants (Jha and Kumar 2006). It can be generated from internal lipid metabolism as an initiator and terminator of lipid peroxidation, or produced in metabolism of the carcinogens N-nitrosopyrrolidine and 1, 3-butadiene (Wang et al. 2017). In the study by Łuczaj et al. (2016), the level of crotonaldehyde in the plasma of healthy subjects was 524.1 ± 341.1 pmol/mL. Crotonaldehyde has been listed as one of nine constituents recommended for disclosure and monitoring by the World Health Organization (WHO) study group on tobacco product regulation (Haussmann 2012). The major environmental exposure routes for crotonaldehyde occur via smog, cigarette smoke, automotive exhaust, and cooking oil fumes. The average urine level of the crotonaldehyde metabolite 3-hydroxy-1-methylpropylmercapturic acid (HPMMA) in 20 smokers was 1857 ± 1379 μg/g (normalized per gram of creatinine)(Goniewicz et al. 2017). It has been reported that crotonaldehyde can rapidly penetrate cell membranes to inhibit intracellular glutathione peroxidase (GPx), causing reactive oxygen species (ROS) accumulation and disequilibrium of oxidative metabolism (Lee et al. 2011; Colombo et al. 2012). As a severe toxic irritant, it can cause eye, skin, and respiratory tract injuries, as well as liver neoplasms. The U.S. Environmental Protection Agency (US EPA) has classified it as a category C chemical (possible human carcinogen), perhaps because chronic exposure to tobacco smoke is a major cause of many respiratory diseases such as chronic obstructive pulmonary disease (COPD), bronchitis, asthma, and lung cancer. Past and present research has focused on the lung toxicity of such air pollutants, but their extra-pulmonary toxic effects have received less attention (Yang et al. 2013a).