ContaminantDB: Malondialdehyde

Identification Taxonomy Biological Properties Physical Properties Toxicity Profile Spectra Concentrations Links References Targets (6)XML

Record Information

Version

1.0

Creation Date

2014-08-29 05:50:41 UTC

Update Date

2026-05-14 17:47:53 UTC

Accession Number

CHEM003142

Identification

Common Name

Malondialdehyde

Class

Small Molecule

Description

Malondialdehyde is a uremic toxin. Uremic toxins can be subdivided into three major groups based upon their chemical and physical characteristics: 1) small, water-soluble, non-protein-bound compounds, such as urea; 2) small, lipid-soluble and/or protein-bound compounds, such as the phenols and 3) larger so-called middle-molecules, such as beta2-microglobulin. Chronic exposure of uremic toxins can lead to a number of conditions including renal damage, chronic kidney disease and cardiovascular disease. Malondialdehyde (MDA) is the dialdehyde of malonic acid and a biomarker of oxidative damage to lipids caused by smoking. Oxidized lipids are able to produce MDA as a decomposition product. The mechanism is thought to involve formation of prostaglandin-like endoperoxides from polyunsaturated fatty acids with two or more double bonds. An alternative mechanism is based on successive hydroperoxide formation and _-cleavage of polyunsaturated fatty acids. MDA is then directly formed by _-scission of a 3-hydroperoxyaldehyde or by reaction between acrolein and hydroxyl radicals. While oxidation of polyunsaturated fatty acids is the major source of MDA in vivo, other minor sources exists such as byproducts of free radical generation by ionizing radiation and of the biosynthesis of prostaglandins. Aldehydes are generally reactive species capable of forming adducts and complexes in biological systems and MDA is no exception although the main species at physiological pH is the enolate ion which is of relative low reactivity. Consistent evidence is available for the reaction between MDA and cellular macromolecules such as proteins, RNA and DNA. MDA reacts with DNA to form adducts to deoxyguanosine and deoxyadenosine which may be mutagenic and these can be quantified in several human tissues. Oxidative stress is an imbalance between oxidants and antioxidants on a cellular or individual level. Oxidative damage is one result of such an imbalance and includes oxidative modification of cellular macromolecules, induction of cell death by apoptosis or necrosis, as well as structural tissue damage. Chemically speaking, oxidants are compounds capable of oxidizing target molecules. This can take place in three ways: abstraction of hydrogen, abstraction of electrons or addition of oxygen. All cells living under aerobic conditions are continuously exposed to a large numbers of oxidants derived from various endogenous and exogenous sources. The endogenous sources of oxidants are several and include the respiratory chain in the mitochondria, immune reactions, enzymes such as xanthine oxidase and nitric oxide synthase and transition metal mediated oxidation. Various exogenous sources of ROS also contribute directly or indirectly to the total oxidant load. These include effects of ionizing and non-ionizing radiation, air pollution and natural toxic gases such as ozone, and chemicals and toxins including oxidizing disinfectants. A poor diet containing inadequate amounts of nutrients may also indirectly result in oxidative stress by impairing cellular defense mechanisms. The cellular macromolecules, in particular lipids, proteins and DNA, are natural targets of oxidation. Oxidants are capable of initiating lipid oxidation by abstraction of an allylic proton from a polyunsaturated fatty acid. This process, by multiple stages leading to the formation of lipid hydroperoxides, is a known contributor to the development of atherosclerosis. (2).

Contaminant Sources

FooDB Chemicals
HMDB Contaminants - Urine
IARC Carcinogens Group 3
T3DB toxins

Contaminant Type

Disinfectant
Food Toxin
Metabolite
Natural Compound
Organic Compound
Pollutant
Uremic Toxin

Chemical Structure

MOL SDF PDB SMILES InChI

Synonyms

Value	Source
1,3-Propanedial	ChEBI
1,3-Propanedialdehyde	ChEBI
1,3-Propanedione	ChEBI
Malonic aldehyde	ChEBI
Malonic dialdehyde	ChEBI
Malonodialdehyde	ChEBI
Malonyldialdehyde	ChEBI
MDA	ChEBI
MDD	ChEBI
Malonaldehyde	HMDB
Propanedial	HMDB
Malondialdehyde, sodium	MeSH, HMDB
Malonylaldehyde	MeSH, HMDB
Sodium malondialdehyde	MeSH, HMDB
Malondialdehyde	ChEBI

Chemical Formula

C₃H₄O₂

Average Molecular Mass

72.063 g/mol

Monoisotopic Mass

72.021 g/mol

CAS Registry Number

542-78-9

IUPAC Name

propanedial

Traditional Name

malonaldehyde

SMILES

O=CCC=O

InChI Identifier

InChI=1S/C3H4O2/c4-2-1-3-5/h2-3H,1H2

InChI Key

WSMYVTOQOOLQHP-UHFFFAOYSA-N

Chemical Taxonomy

Description

belongs to the class of organic compounds known as 1,3-dicarbonyl compounds. These are carbonyl compounds with the generic formula O=C(R)C(H)C(R')=O, where R and R' can be any group.

Kingdom

Organic compounds

Super Class

Organic oxygen compounds

Class

Organooxygen compounds

Sub Class

Carbonyl compounds

Direct Parent

1,3-dicarbonyl compounds

Alternative Parents

Substituents

1,3-dicarbonyl compound
Alpha-hydrogen aldehyde
Organic oxide
Hydrocarbon derivative
Short-chain aldehyde
Aldehyde
Aliphatic acyclic compound

Molecular Framework

Aliphatic acyclic compounds

External Descriptors

dialdehyde (CHEBI:566274 )

Biological Properties

Status

Detected and Not Quantified

Origin

Endogenous

Cellular Locations

Cytoplasm
Extracellular

Biofluid Locations

Not Available

Tissue Locations

Not Available

Pathways

Not Available

Applications

biomarker

Biological Roles

Not Available

Chemical Roles

Not Available

Physical Properties

State

Solid

Appearance

White powder.

Experimental Properties

Property	Value
Melting Point	72°C
Boiling Point	Not Available
Solubility	Not Available

Predicted Properties

Property	Value	Source
Water Solubility	241 g/L	ALOGPS
logP	0.1	ALOGPS
logP	-0.65	ChemAxon
logS	0.52	ALOGPS
pKa (Strongest Acidic)	6.68	ChemAxon
pKa (Strongest Basic)	-6.8	ChemAxon
Physiological Charge	-1	ChemAxon
Hydrogen Acceptor Count	2	ChemAxon
Hydrogen Donor Count	0	ChemAxon
Polar Surface Area	34.14 Å²	ChemAxon
Rotatable Bond Count	2	ChemAxon
Refractivity	17.14 m³·mol⁻¹	ChemAxon
Polarizability	6.42 Å³	ChemAxon
Number of Rings	0	ChemAxon
Bioavailability	1	ChemAxon
Rule of Five	Yes	ChemAxon
Ghose Filter	No	ChemAxon
Veber's Rule	Yes	ChemAxon
MDDR-like Rule	No	ChemAxon

Spectra

Spectrum Type	Description	Splash Key	View
Predicted GC-MS	Predicted GC-MS Spectrum - GC-MS (Non-derivatized) - 70eV, Positive	splash10-006x-9000000000-f27c7e0c26f7fd9a353b	Spectrum
Predicted GC-MS	Predicted GC-MS Spectrum - GC-MS (Non-derivatized) - 70eV, Positive	Not Available	Spectrum
Predicted LC-MS/MS	Predicted LC-MS/MS Spectrum - 10V, Positive	splash10-00di-9000000000-744a9fd4b0afe1939db8	Spectrum
Predicted LC-MS/MS	Predicted LC-MS/MS Spectrum - 20V, Positive	splash10-05fr-9000000000-38c741cd3f463e2fdbb3	Spectrum
Predicted LC-MS/MS	Predicted LC-MS/MS Spectrum - 40V, Positive	splash10-0a4i-9000000000-18018045cdfb4fd65e5b	Spectrum
Predicted LC-MS/MS	Predicted LC-MS/MS Spectrum - 10V, Negative	splash10-00di-9000000000-bd4fb7676d96faa15028	Spectrum
Predicted LC-MS/MS	Predicted LC-MS/MS Spectrum - 20V, Negative	splash10-00di-9000000000-45f19081a5a0a9b81852	Spectrum
Predicted LC-MS/MS	Predicted LC-MS/MS Spectrum - 40V, Negative	splash10-0ukc-9000000000-01e3136b16e8f53d525c	Spectrum
Predicted LC-MS/MS	Predicted LC-MS/MS Spectrum - 10V, Positive	splash10-0006-9000000000-3d8581e7b0d371dd2923	Spectrum
Predicted LC-MS/MS	Predicted LC-MS/MS Spectrum - 20V, Positive	splash10-052f-9000000000-2a7f481a2402d9628b46	Spectrum
Predicted LC-MS/MS	Predicted LC-MS/MS Spectrum - 40V, Positive	splash10-0a4i-9000000000-5846b4edd05c82b946ec	Spectrum
Predicted LC-MS/MS	Predicted LC-MS/MS Spectrum - 10V, Negative	splash10-00di-9000000000-85ee1d7f8db31720e3cf	Spectrum
Predicted LC-MS/MS	Predicted LC-MS/MS Spectrum - 20V, Negative	splash10-0006-9000000000-c9a8aeda6f81e0b439e2	Spectrum
Predicted LC-MS/MS	Predicted LC-MS/MS Spectrum - 40V, Negative	splash10-0006-9000000000-6269ba171aca8de72e5f	Spectrum
1D NMR	13C NMR Spectrum	Not Available	Spectrum
1D NMR	1H NMR Spectrum	Not Available	Spectrum
1D NMR	13C NMR Spectrum	Not Available	Spectrum
1D NMR	1H NMR Spectrum	Not Available	Spectrum
1D NMR	13C NMR Spectrum	Not Available	Spectrum
1D NMR	1H NMR Spectrum	Not Available	Spectrum
1D NMR	13C NMR Spectrum	Not Available	Spectrum
1D NMR	1H NMR Spectrum	Not Available	Spectrum
1D NMR	13C NMR Spectrum	Not Available	Spectrum
1D NMR	1H NMR Spectrum	Not Available	Spectrum
1D NMR	13C NMR Spectrum	Not Available	Spectrum
1D NMR	1H NMR Spectrum	Not Available	Spectrum
1D NMR	13C NMR Spectrum	Not Available	Spectrum
1D NMR	1H NMR Spectrum	Not Available	Spectrum
1D NMR	13C NMR Spectrum	Not Available	Spectrum
1D NMR	1H NMR Spectrum	Not Available	Spectrum
1D NMR	13C NMR Spectrum	Not Available	Spectrum
1D NMR	1H NMR Spectrum	Not Available	Spectrum
1D NMR	13C NMR Spectrum	Not Available	Spectrum
1D NMR	1H NMR Spectrum	Not Available	Spectrum

Toxicity Profile

Route of Exposure

Endogenous, Ingestion, Dermal (contact)

Mechanism of Toxicity

Uremic toxins such as malondialdehyde are actively transported into the kidneys via organic ion transporters (especially OAT3). Increased levels of uremic toxins can stimulate the production of reactive oxygen species. This seems to be mediated by the direct binding or inhibition by uremic toxins of the enzyme NADPH oxidase (especially NOX4 which is abundant in the kidneys and heart) (3). Reactive oxygen species can induce several different DNA methyltransferases (DNMTs) which are involved in the silencing of a protein known as KLOTHO. KLOTHO has been identified as having important roles in anti-aging, mineral metabolism, and vitamin D metabolism. A number of studies have indicated that KLOTHO mRNA and protein levels are reduced during acute or chronic kidney diseases in response to high local levels of reactive oxygen species (4).

Metabolism

Uremic toxins tend to accumulate in the blood either through dietary excess or through poor filtration by the kidneys. Most uremic toxins are metabolic waste products and are normally excreted in the urine or feces.

Toxicity Values

Not Available

Lethal Dose

Not Available

Carcinogenicity (IARC Classification)

3, not classifiable as to its carcinogenicity to humans. (5)

Uses/Sources

Naturally produced by the body (endogenous).

Minimum Risk Level

Not Available

Health Effects

Chronic exposure to uremic toxins can lead to a number of conditions including renal damage, chronic kidney disease and cardiovascular disease.

Symptoms

As a uremic toxin, this compound can cause uremic syndrome. Uremic syndrome may affect any part of the body and can cause nausea, vomiting, loss of appetite, and weight loss. It can also cause changes in mental status, such as confusion, reduced awareness, agitation, psychosis, seizures, and coma. Abnormal bleeding, such as bleeding spontaneously or profusely from a very minor injury can also occur. Heart problems, such as an irregular heartbeat, inflammation in the sac that surrounds the heart (pericarditis), and increased pressure on the heart can be seen in patients with uremic syndrome. Shortness of breath from fluid buildup in the space between the lungs and the chest wall (pleural effusion) can also be present.

Treatment

Kidney dialysis is usually needed to relieve the symptoms of uremic syndrome until normal kidney function can be restored.

Concentrations

Not Available

External Links

DrugBank ID

DB03057

HMDB ID

HMDB0006112

FooDB ID

FDB008116

Phenol Explorer ID