China 
Africa 
Explore chapters and articles related to this topic
Omics Approaches for the Production of the Microbial Enzymes and Applications
Published in Pankaj Bhatt, Industrial Applications of Microbial Enzymes, 2023
Heena Parveen, Anuj Chaudhary, Parul Chaudhary, Rabiya Sultana, Govind Kumar, Priyanka Khati, Meenakshi Rana, Pankaj Bhatt
Dehydrogenases are oxidoreductases that can be found in bacteria, yeast, plants, and animals [30–34]. Dehydrogenases use a coenzyme like NAD+/NADP+ as an electron acceptor to catalyze the oxidation-reduction reaction. Alcohol dehydrogenase enzymes convert alcohol into aldehydes or ketones. Other aromatic dehydrogenases reported include naphthalene dihydrodiol dehydrogenase, polyethylene glycol dehydrogenase, benzyl alcohol dehydrogenase, and others [35]. Previously, bacterial cell-free extracts digest the industrially generated xenobiotics of various molecular weights, and the polyethylene glycol dehydrogenase activity was detected [36]. Similarly, another dehydrogenase, dye-linked polypropene glycol dehydrogenase in the periplasm or membrane of Stenotrophomonas maltophilia, is energetic in high-molecular-weight PPG degradation, whereas a cytoplasm-located enzyme was found to be active in hydrolyzing low-molecular-weight composite [37]. In a recent study, a novel dehydrogenase, 17β-hydroxysteroid dehydrogenase (17β-HSDx) present in Rhodococcus sp. P14, showed better activity in steroid bioremediation [38]. In previous studies, Rhodococcus sp. was originally involved in the degradation of various polycyclic aromatic hydrocarbons.
Conversion of Natural Products from Renewable Resources in Pharmaceuticals by Cytochromes P450
Published in Peter Grunwald, Pharmaceutical Biocatalysis, 2019
Giovanna Di Nardo, Gianfranco Gilardi
Mammalian cytochromes P450 have also been used as biocatalyst for steroid hydroxylation in yeast recombinant systems. In the late 1990s, the self-sufficient biosynthesis of pregnenolone and progesterone were achieved by engineering six genes in Saccaromyces cerevisiae (Duport et al., 1998). The bovine cytochrome P450 11A1 was introduced, together with the redox partner, in the fungus engineered to accumulate ergosta-5-ene-ol and ergosta-5,22-diene-ol from the endogenous ergosterol. The two compounds are substrates of P450 11A1, which produces pregnenolone, which is then converted to progesterone through the action of 3-β-hydroxysteroid dehydrogenase.
Human Health Risk Assessment of Perfluorinated Chemicals
Published in David M. Kempisty, Yun Xing, LeeAnn Racz, Perfluoroalkyl Substances in the Environment, 2018
The adverse effects of PFOA in the testes of mice were noted in both WT and humanized PPAR-α mice, but not in KO mice, indicating these effects were mediated by PPAR-α activation (Li et al., 2011). Direct inhibition of steroidogenesis in Leydig cells may also play a significant role in the observed toxicity, as PFOA, PFDA, and PFDoDA inhibited steroidogenesis in primary Leydig cells derived from adult rats and in Leydig cell tumor lines (Biegel et al., 1995; Boujrad et al., 2000; Shi et al., 2010) via competitive inhibition of steroidogenic enzymes and also possibly downregulation of steroidogenic gene expression. PFAS reportedly inhibited human 17β-hydroxysteroid dehydrogenase 3 (17βHSD3) and rat 3β-hydroxysteroid dehydrogenase (3βHSD3), two enzymes critical to the conversion of cholesterol to testosterone in Leydig cells; the IC50 values for PFOS inhibition of rat 3βHSD3 and human 17βHSD3 were 1.35 and 6.02 μM, respectively (Zhao et al., 2010b). This study also reported that the IC50 value for inhibition of 17βHSD3 by PFOA was 127.6 μM; PFAS preferentially inhibited rat 3βHSD3, while human 17βHSD3 was more sensitive to PFAS inhibition than human 3βHSD3. Antagonist activity at the androgen receptor may also play a role in the observed toxicity, as PFOS, PFOA, PFNA, PFDA, and PFHxS inhibited dihydrotestosterone activity at the androgen receptor at a concentration range of 4.7–52 μM, which is 100- to 1000-fold less potent than flutamide (Kjeldsen and Bonefeld-Jorgensen, 2013). Finally, indicators of cell damage, such as lipid accumulation and ROS accumulation in mitochondria, were also noted in Leydig cells treated with PFAS (Boujrad et al., 2000; Shi et al., 2010), indicating that direct PFAS induction of oxidative stress may act synergistically to exacerbate the effects of hormone synthesis disruption on the testes.
The toxic contaminants of Aspalathus linearis plant material as well as herb–drug interactions may constitute the health risk factors in daily rooibos tea consumers
Published in International Journal of Environmental Health Research, 2023
Moreover, other metabolizing enzymes may be involved. Marnewick et al. (2003) reported that unoxidized rooibos potentiates in rats the activity of the hepatic second phase enzymes (UDP-glucuronosyltransferase and glutathione-S-transferase) that play a role in glucuronidation reactions transforming lipophilic drugs into more polar metabolites as well as catalyze the conjugation of reduced glutathione to electrophilic substrates. Abrahams et al. (2019) showed that aspalathin-enriched ‘unfermented’ extract also modulated the expression of some genes encoding polyphenol-metabolizing enzymes. In the rat liver, the upregulation of the genes of aldehyde dehydrogenase, glucose phosphate isomerase and cytochrome P450 as well as downregulation of 17β-hydroxysteroid dehydrogenase type 2 were observed, whereas in the culture of primary hepatocytes only aspalathin itself provoked similar CYP and 17β-hydroxysteroid dehydrogenase type 2 (17βHSD2) changes. These interactions suggest, e.g. improved alcohol metabolism and interaction with steroid hormones, resulting in the smaller breakdown of estradiol, testosterone and 5α-DHT in the liver as well as enhanced estrogen production. Besides Schloms et al. (2014) reported glucocorticoid synthesis and metabolism affected by rooibos extract in the mechanism of the 11β-hydroxysteroid dehydrogenase type 1 (11βHSD1) inhibition, resulting in a decreased cortisol:cortisone ratio. The interference of rooibos tea with hepatic metabolism based on available research is gathered in Figure 3.
Two modified density gradient centrifugation methods facilitate the isolation of mouse Leydig cells
Published in Preparative Biochemistry & Biotechnology, 2023
Jiayang Jiang, Xiaoman Zhou, Chunliu Gao, Rongqin Ke, Qiwei Guo
To evaluate the purity of the LCs, 3β-hydroxysteroid dehydrogenase (HSD3B) staining was performed. HSD3B is an LC-specific marker involved in steroid progesterone biosynthesis.[16] Positively stained LCs are bluish violet in color and can be distinguished from other cell populations. Staining was performed as described previously.[17,18] Briefly, 20 μL of diluted cells were placed on a slide and dried at room temperature for 1 h. The dried film was incubated with staining solution for 60 min at 36 °C. The proportions of LCs were evaluated by light microscopy (Olympus, Tokyo, Japan). Three independent microscope fields (∼50–150 cells per field) were used for the cell counting. To evaluate the yields of LCs, purified cells were quantified using a hemocytometer (Marienfeld) and LC yield was measured by multiplying the number of purified cells by the proportions of LCs.
Urinary Isoflavones Levels in Relation to Serum Thyroid Hormone Concentrations in Female and Male Adults in the U.S. General Population
Published in International Journal of Environmental Health Research, 2021
Patricia A. Janulewicz, Jeffrey M. Carlson, Amelia K. Wesselink, Lauren A. Wise, Elizabeth E. Hatch, Lariah M. Edwards, Junenette L. Peters
Alternatively, isoflavones may inhibit the body’s ability to bind free T4, resulting in elevated endogenous concentrations. Previous studies among premenopausal women suggest that increases in dietary isoflavones are inversely associated with both estrone (Nagata et al. 1998) and estradiol (Lu et al. 1996, 2000; Nagata et al. 1997; Xu et al. 1998; Wu et al. 2000). This may occur because phytoestrogens can act as aromatase, sulfatase, and 17 ß-hydroxysteroid dehydrogenase inhibitors (Figure 2), preventing the conversion of androgens to estrogens (Wang et al. 1994; Lephart 2015). Low estrogen levels may reduce levels of thyroxine binding globulin (TBG) (Ain et al. 1987; Duncan et al. 1999), which in turn can decrease free T4 (Dillingham et al. 2007; Lee et al. 2009). Low estrogen levels in males could explain the lower levels of free T4 we found in males but not in females associated with isoflavone exposure. This could also explain the positive results seen for daidzein, genistein and O-DMA but not for equol.