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Biocatalytic Reduction of Organic Compounds by Marine-Derived Fungi
Published in Se-Kwon Kim, Marine Biochemistry, 2023
Gabriel S. Baia, David E. Q. Jimenez, André Luiz Meleiro Porto
The aldo-keto reductase (AKR) enzymes can catalyze asymmetric reductions of carbonyl compounds. The difference between ERs and AKRs is that the latter needs coenzymes, for example, nicotinamide adenine dinucleotide (NADH), nicotinamide adenine dinucleotide phosphate (NADPH) and flavin [14]. The carbonyl group reduction proceeds in two steps: (1) the hydroxyl group of the substrate is reduced, and the coenzyme is oxidized to NAD(P)+, and (2) the NAD(P)+ and alcohol product system are dissociated from the enzyme. Sheng et al. (2019) described the use of AKRs by perakine reductase in the reduction of (E)-4-phenylbut-3-en-2-one to (S,E)-4-phenylbut-3-en-2-ol. The reduction reaction conditions were 30°C and 150 rpm in Kpi buffer for 10 h. AKR affords the alcohol product in 60% yield and >99% ee of the S-enantiomer as shown in Figure 15.6 [15].
Effects of cross-fostering and developmental exposure to mixtures of environmental contaminants on hepatic gene expression in prepubertal 21 days old and adult male Sprague-Dawley rats
Published in Journal of Toxicology and Environmental Health, Part A, 2019
D. Desaulniers, N. Khan, C. Cummings-Lorbetskie, K. Leingartner, G-H. Xiao, A. Williams, C.L. Yauk
DEG at PND78-86 indicated altered retinoid metabolism and bile acid biosynthesis. Akr1c1 (AKR1C4 in human), Akr1c2 (AKR1C1 in human) and murine-specific Akr1c12, were down-regulated (indicative of cholesterol and bile acid metabolism deregulation), while Sdr16c6 was up-regulated in the M group, potentially contributing to altered retinoid metabolism. These aldo-keto reductase transcripts (AKR families) are phase I metabolizing enzymes that catalyze conversion of aldehydes and ketones to their corresponding alcohols, and thus reduce a variety of lipophilic substrates including xenobiotics, steroids, prostaglandins, bile acids, and retinoids (Rizner and Penning 2014; Ruiz et al. 2012). In the opposite enzymatic direction, the short-chain dehydrogenase/reductase SDR16C family members (Sdr16c6 up-regulated here) are thought to oxidize retinol to retinaldehyde (Adams et al. 2017). Depletion of vitamin-A (fat soluble retinoids) is one of the most sensitive markers of exposure to TCDD (Fletcher, Hanberg, and Håkansson 2001). Morse and Brouwer (1995) noted effects on the retinoid system until at least PND90 after gestational exposure to the highly toxic PCB mixture Aroclor 1254 at doses of 5 or 25 mg/kg body weight. Using a mixture similar to ours, Elabbas et al. (2014) observed decreased abundance of hepatic retinol in the livers of male offspring at PND35, but increased abundance at intermediate doses (0.05 and 0.5 mg/kg/day) relative to control in both F1 males and females at PND77. The persistent deregulation of retinoid metabolism and its health impacts warrants further investigation.