17β-Hydroxysteroid dehydrogenase type 8 (17β-HSD8) plays a pivotal role in the metabolism of steroids, a class of compounds essential for a wide range of biological functions. As an enzyme, 17β-HSD8 is critical in the biosynthesis and transformation of various hormones, including the interconversion between less active and more active forms of estrogens and androgens. The modulation of this enzyme's expression is a complex process influenced by a myriad of factors within the cellular environment. Changes in the expression levels of 17β-HSD8 can have significant effects on the balance and availability of hormones, which is a tightly regulated aspect of human physiology. Given the enzyme's role in these fundamental processes, understanding the substances that can induce its expression is of considerable interest in the field of biochemical research.
Several chemical compounds have been identified that might lead to the induction of 17β-HSD8 expression. These include various environmental, dietary, and endogenous substances. For instance, Bisphenol A (BPA), a chemical found in many consumer products, may mimic the structure and function of estrogen, potentially leading to an increase in the expression of enzymes such as 17β-HSD8. Similarly, phthalates, which are used as plasticizers, might disrupt the endocrine system's normal functioning, resulting in an upsurge in 17β-HSD8 to maintain the body's hormonal balance. Environmental contaminants like polychlorinated biphenyls (PCBs) and dioxins can cause alterations in steroid hormone levels, which, in turn, could trigger the body's mechanisms to upregulate 17β-HSD8. Metals like arsenic, cadmium, and lead are known to induce oxidative stress and may stimulate the expression of detoxifying enzymes including 17β-HSD8, as part of the cellular defense response. These findings elucidate the intricate network of interactions where 17β-HSD8 is a key player, reflecting the enzyme's responsiveness to a broad spectrum of substances.
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| Product Name | CAS # | Catalog # | QUANTITY | Price | Citations | RATING |
|---|---|---|---|---|---|---|
Bisphenol A | 80-05-7 | sc-391751 sc-391751A | 100 mg 10 g | $300.00 $490.00 | 5 | |
Bisphenol A, due to its structural similarity to estrogen, may mimic estrogenic activity, potentially stimulating the upregulation of steroidogenic enzymes such as 17β-HSD8. | ||||||
Bis(2-ethylhexyl) phthalate | 117-81-7 | sc-254975 | 1 g | $57.00 | 2 | |
This phthalate may disrupt normal hormonal signaling, leading to a compensatory increase in the synthesis of enzymes like 17β-HSD8 to maintain hormonal homeostasis. | ||||||
Insulin | 11061-68-0 | sc-29062 sc-29062A sc-29062B | 100 mg 1 g 10 g | $156.00 $1248.00 $12508.00 | 82 | |
Insulin can stimulate the synthesis of various enzymes involved in lipid and steroid metabolism, possibly leading to an increase in 17β-HSD8 expression to aid in these processes. | ||||||
Metformin | 657-24-9 | sc-507370 | 10 mg | $79.00 | 2 | |
Metformin's action on cellular metabolism may include stimulating the transcriptional activity of genes encoding enzymes like 17β-HSD8, to facilitate its role in energy regulation. | ||||||
Retinoic Acid, all trans | 302-79-4 | sc-200898 sc-200898A sc-200898B sc-200898C | 500 mg 5 g 10 g 100 g | $66.00 $325.00 $587.00 $1018.00 | 28 | |
Retinoic acid, through its role as an active metabolite of vitamin A, can induce gene transcription and may specifically stimulate the upregulation of 17β-HSD8 in steroidogenic tissues. | ||||||
Tributyltin hydride | 688-73-3 | sc-255686 sc-255686A | 10 g 50 g | $69.00 $192.00 | ||
Tributyltin, as an organotin compound, can interfere with fatty acid metabolism and mitochondrial function, potentially leading to an upsurge in 17β-HSD8 expression as a compensatory mechanism. | ||||||
Arsenic sponge | 7440-38-2 | sc-278710 | 25 g | $236.00 | ||
Arsenic exposure has been associated with oxidative stress and may elicit a cellular response that includes the upregulation of detoxifying enzymes such as 17β-HSD8. | ||||||
Lead | 7439-92-1 | sc-250236 | 2 kg | $104.00 | ||
Lead's interference with calcium-dependent signaling pathways may prompt an upregulation of 17β-HSD8 expression as a compensatory response to mitigate lead toxicity. | ||||||