Table 4.
Properties | References |
---|---|
Physiological substrates: 25- and 27-Hydroxycholesterol, pregnenolone, dehydroepiandrosterone (DHEA), epiandrosterone, 5α-androstane-3β,17β-diol, estrone | (Rose et al. 1997; Steckelbroeck et al. 2002; Kim SB et al. 2004; Stiles et al. 2009; Yantsevich et al. 2014; Pan et al. 2016) |
Function: 25-Hydroxycholesterol 7α-hydroxylase, oxysterol and steroid 6α- or 7α-hydroxylase (Fig. 6); involved in metabolism of neurosteroids (brain), bile acid synthesis (liver), and metabolism of estrogen receptor ligands (in prostate) |
|
Inhibition: Possible liver failure and progressive neuropathy | |
Inhibitors: | |
Drugs: | |
Imidazole and triazole drugs (ketoconazole, bifoconazole, miconazole, clotrimazole, econazole, fluconazole, tioconazole, voriconazole) a (Kim SB et al. 2004; Yantsevich et al. 2014) | |
Metyrapone a (Yantsevich et al. 2014) | |
Physiological compounds: | |
5α-Androstane-3β,17β-diol, estrone, testosterone, 17β-estradiol b (Kim SB et al. 2004; Tang et al. 2006; Pettersson et al. 2008) | |
5α-Dihydrotestosterone b (at high concentrations) (Pettersson et al. 2008) | |
Estrogens (estrone, 17β-estradiol–in the absence of estrogen receptor α) b (Tang et al. 2006) | |
Triiodothyronine c (T3) (Ellis 2006) | |
β-Amyloid peptide (non-competitive inhibition) (Kim SB et al. 2004) | |
Physiological condition and illnesses: | |
Breast cancer d (Wu et al. 2013) | |
Prostatic cancer d (in type 2 diabetes) (Lutz et al. 2018) | |
Other compounds: | |
Pesticides a (tebuconazole, propiconazole) (Yantsevich et al. 2014) | |
Induction: Immunostimulatory effect of 7α-hydroxydehydroepiandosterone (used in rheumatoid artritis) | |
Inducers: | |
Drugs: | |
Rifampicin (Kim B et al. 2013) | |
Physiological compounds: | |
17β-Estradiol e (in human embryonic kidney (HEK293) cells transfected with estrogen receptor α) (Dulos, van der Vleuten, et al. 2005; Tang et al. 2006) | |
Interleukin-1 β interleukin-1α, interleukin-7, interleukin-17, activator protein-1, nuclear factor–κΒ, tumor necrosis factor-α e (Dulos, Kaptein, et al. 2005; Dulos, van der Vleuten, et al. 2005; Dulos and Boots 2006) | |
Physiological condition and illnesses: | |
Prostatic cancer f (Olsson et al. 2007) | |
Psoriasis f (Sumantran et al. 2016) | |
Other compounds: | |
Oleic acid anilide e (An et al. 2008) |
Footnotes:
Competitive inhibition, ligand binding
Decreased/suppressed/inhibited activity/product formation
Reduced/suppressed mRNA and/or protein level/expression and activity
Gene downregulated/suppressed
Increased transcription/mRNA/protein expression/levels /and/or catalytic activity
Up-regulation of biosynthesis, increased expression of protein