Alcohol Dehydrogenase 1 (Adh1) is a pivotal enzyme in the metabolic process, primarily involved in the catalysis of alcohol to its corresponding aldehyde or ketone. The enzyme plays a critical role in the metabolism of various alcohols within the body, facilitating their conversion into substances that can be further broken down and utilized for energy or excreted. The expression of Adh1 is a tightly controlled biological process, sensitive to alterations in metabolic demands and exposure to different substrates and environmental factors. As such, various compounds can induce the expression of Adh1, leading to an increase in the enzyme's levels within cells, a process that is essential for maintaining metabolic homeostasis.
Compounds that can potentially induce the expression of Adh1 include a diverse array of chemicals, each interacting with cellular mechanisms to stimulate the production of this enzyme. For instance, ethanol, the very substrate that Adh1 acts upon, can enhance the enzyme's expression. This phenomenon is thought to be a compensatory response, allowing cells to efficiently process and detoxify an excess of alcohol. Other compounds, such as retinoic acid, have a more regulatory role, influencing gene transcription through interaction with nuclear receptors and response elements on DNA that control the synthesis of Adh1. Environmental stressors, including exposure to heavy metals like lead and cadmium, can also lead to an upsurge in Adh1 expression as part of the cellular defense system to counteract oxidative stress and preserve cellular integrity. Organic solvents such as chloroform are metabolized by Adh1; hence, exposure to such compounds can trigger an increase in enzyme levels to facilitate their metabolism. Collectively, these activators, ranging from alcohols to metal ions and organic compounds, highlight the adaptive capacity of cellular enzyme regulation in response to both endogenous and exogenous stimuli.
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| Product Name | CAS # | Catalog # | QUANTITY | Price | Citations | RATING |
|---|---|---|---|---|---|---|
Retinoic Acid, all trans | 302-79-4 | sc-200898 sc-200898A sc-200898B sc-200898C | 500 mg 5 g 10 g 100 g | $65.00 $319.00 $575.00 $998.00 | 28 | |
Retinoic acid can initiate transcriptional activation of Adh1 through binding to nuclear receptors, which then bind to retinoic acid response elements in the promoter region of the gene. | ||||||
Lead(II) Acetate | 301-04-2 | sc-507473 | 5 g | $83.00 | ||
Lead(II) acetate can trigger the upregulation of Adh1 as part of a cellular defense mechanism to mitigate oxidative stress caused by heavy metal exposure. | ||||||
Benzene | 71-43-2 | sc-239290 | 1 L | $77.00 | ||
Exposure to benzene can stimulate the induction of Adh1 expression as the enzyme plays a role in detoxifying benzene metabolites. | ||||||
Isoniazid | 54-85-3 | sc-205722 sc-205722A sc-205722B | 5 g 50 g 100 g | $25.00 $99.00 $143.00 | ||
Isoniazid can upregulate Adh1 expression by increasing the hepatic demand for acetaldehyde metabolism during its biotransformation. | ||||||
Fomepizole | 7554-65-6 | sc-252838 | 1 g | $74.00 | 1 | |
Fomepizole administration can lead to an upregulation of Adh1 as the body enhances its enzymatic mechanisms to counteract poisoning by substances like ethylene glycol. | ||||||
Sodium (meta)arsenite | 7784-46-5 | sc-250986 sc-250986A | 100 g 1 kg | $106.00 $765.00 | 3 | |
Sodium (meta)arsenite exposure can stimulate an adaptive increase in Adh1 expression as the enzyme is involved in the metabolism of arsenite-induced oxidative products. | ||||||
Cadmium chloride, anhydrous | 10108-64-2 | sc-252533 sc-252533A sc-252533B | 10 g 50 g 500 g | $55.00 $179.00 $345.00 | 1 | |
Cadmium chloride can provoke an increase in Adh1 gene expression as part of a broader cellular response to heavy metal stress, aiming to preserve cell viability. | ||||||
Chloroform | 67-66-3 | sc-239527A sc-239527 | 1 L 4 L | $110.00 $200.00 | 1 | |
Chloroform can lead to an elevation in Adh1 expression levels as the liver attempts to enhance the metabolism of this volatile organic compound to less harmful metabolites. | ||||||