3,4-Dihydroxybenzeneacetic acid

From NuGOwiki

(Redirected from HMDB01336)

The NuGOwiki Metabolite Database is a joint initiative of NuGO and HMDB

Taxonomy Navigation Box; search by

3,4-Dihydroxybenzeneacetic acid
2D structure for 3,4-Dihydroxybenzeneacetic acid
Chemical Name	2-(3,4-dihydroxyphenyl)acetic acid
Chemical Formula	C₈H₈O₄
CAS Number	102-32-9
Chemical Information	HMDB01336
Biochemical Taxonomy	Aromatic Acids
Functional Taxonomy	Not Available
Nutritional Taxonomy	Not Available
Metabolic Pathways	Glycolysis
Biofluid Location	Blood Cerebrospinal Fluid (CSF) Urine
Tissue Location	Hypothalamus Neurons Striatum Brain
Normal Biofluid Concentrations	Blood: 0.019 +/- 0.009 umol/L Cerebrospinal Fluid (CSF): 0.0001 +/- 0.00002 uM Cerebrospinal Fluid (CSF): 0.002 +/- 0.001 (0.001 - 0.003) uM Cerebrospinal Fluid (CSF): 0.003 +/- 0.0015 (0.0013 - 0.0045) uM Urine: 0.48 +/- 0.4 umol/mmol creatinine
Normal Tissue Concentrations	Not Available
Diseases / Conditions Related to Nutrition	Alzheimer's Disease Encephalitis patients Hypothyroidism
Other (Monogenic Disorders)	Not Available
Abnormal Biofluid Concentrations	Cerebrospinal Fluid (CSF) (Alzheimer's Disease): 0.0023 +/- 0.0015 (0.00051-0.0042) uM Cerebrospinal Fluid (CSF) (Encephalitis patients): 0.01 +/- 0.003 uM Cerebrospinal Fluid (CSF) (Hypothyroidism): 0.0001 (0.000070-0.00013) uM Cerebrospinal Fluid (CSF) (Hypothyroidism): 0.0001 +/- 0.00003 uM
Abnormal Tissue Concentrations	Not Available
Physiological Processes	Not Available

Authors:
Affiliations:

Introduction

guidelines
3,4-dihydroxyphenylacetic acid (DOPAC) is a phenolic acid. DOPAC is a neuronal metabolite of dopamine (DA). DA undergoes monoamine oxidase-catalyzed oxidative deamination to 3,4-dihydroxyphenylacetaldehyde (DOPAL), which is metabolized primarily to DOPAC via aldehyde dehydrogenase (ALDH2). The biotransformation of DOPAL is critical as previous studies have demonstrated this DA-derived aldehyde to be a reactive electrophile and toxic to dopaminergic cells. Known inhibitors of mitochondrial ALDH2, such as 4-hydroxy-2-nonenal (4HNE) inhibit ALDH2-mediated oxidation of the endogenous neurotoxin DOPAL. 4HNE is one of the resulting products of oxidative stress, thus linking oxidative stress to the uncontrolled production of an endogenous neurotoxin relevant to Parkinson's disease. In early onset Parkinson disease there is markedly reduced activities of both monoamine oxidase (MAO) A and B. The amount of DOPAC, which is produced during dopamine oxidation by MAO, is greatly reduced as a result of increased parkin overexpression. Administration of methamphetamine to animals causes loss of DA terminals in the brain, and significant decreases in Dopamine and dihydroxyphenylacetic acid (DOPAC) in the striata. Renal dopamine produced in the residual tubular units may be enhanced during a sodium challenge, thus behaving appropriately as a compensatory natriuretic hormone; however the renal dopaminergic system in patients afflicted with renal parenchymal disorders should address parameters other than free urinary dopamine, namely the urinary excretion of L-DOPA and metabolites. DOPAC is one of the major phenolic acids formed during human microbial fermentation of tea, citrus, and soy flavonoid supplements. DOPAC exhibits a considerable antiproliferative effect in LNCaP prostate cancer and HCT116 colon cancer cells. The antiproliferative activity of DOPAC may be due to its catechol structure. A similar association of the catechol moiety in the B-ring with antiproliferative activity was demonstrated for flavanones. (PMID: 16956664, 16455660, 8561959, 11369822, 10443478, 16365058)