malondialdehyde (MDA)


OTHER NAMES:
propanedial


ABBREVIATIONS:
MDA


DESCRIPTION: Malondialdehyde is a naturally occurring product of lipid peroxidation and prostaglandin biosynthesis which is mutagenic and carcinogenic. It reacts with DNA to form adducts to deoxyguanosine and deoxyadenosine. The major adduct to DNA is a pyrimidopurinone called pyrimido[1,2-a]purin-10(3H)-one (M1G). Studies of site-specific mutagenesis indicate that M1G is mutagenic in bacteria and is repaired by the nucleotide excision repair pathway. M1G has been detected in liver, leukocytes, pancreas and breast from healthy human beings at levels ranging from 1 to 120 per 10(8) nucleotides. 

Reactive oxygen species degrade polyunsaturated lipids, forming malondialdehyde. This compound is a reactive aldehyde and is one of the many reactive electrophile species that cause toxic stress in cells and form covalent protein adducts referred to as advanced lipoxidation end-products (ALE), in analogy to advanced glycation end-products (AGE). The production of this aldehyde is used as a biomarker to measure the level of oxidative stress in an organism.
Malonaldehyde reacts with deoxyadenosine and deoxyguanosine in DNA, forming DNA adducts, the primary one being M1G, which is mutagenic. The guanidine group of arginine residues condense with MDA to give 2-aminopyrimidines.

Malonaldehyde is the organic compound with the formula CH2(CHO)2. The structure of this species is more complex than this formula suggests. This reactive species occurs naturally and is a marker for oxidative stress.

DNA DAMAGES:
M1A (OPA)
M3C
M1dG
M3dA
M1C (OPC)
M2G


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NAME STRUCTURE PROTEINS DNA DAMAGE EFFECT(S) PATHWAY(S) RELATED
M1A (OPA) UvrC
UvrB
ERCC5 (XPG)
ERCC4 (XPF)
A→G transition
carcinogen
mutagenesis
transition
Fanconi anemia (FA) pathway
nucleotide excision repair (NER)
prokaryotic (SOS) response
M3C UvrC
UvrB
ERCC5 (XPG)
ERCC4 (XPF)
carcinogen
mutagenesis
Fanconi anemia (FA) pathway
nucleotide excision repair (NER)
prokaryotic (SOS) response
M1dG UvrC
UvrB
ERCC5 (XPG)
ERCC4 (XPF)
carcinogen
G→A transition
G→C transversion
G→T transversion
mutagenesis
point mutation
substitution
transition
transversion
Fanconi anemia (FA) pathway
nucleotide excision repair (NER)
prokaryotic (SOS) response
M3dA UvrC
UvrB
ERCC5 (XPG)
ERCC4 (XPF)
carcinogen
mutagenesis
Fanconi anemia (FA) pathway
nucleotide excision repair (NER)
prokaryotic (SOS) response
M1C (OPC) UvrC
UvrB
ERCC5 (XPG)
ERCC4 (XPF)
carcinogen
C→T transition
mutagenesis
transition
Fanconi anemia (FA) pathway
nucleotide excision repair (NER)
prokaryotic (SOS) response
M2G UvrC
UvrB
ERCC5 (XPG)
ERCC4 (XPF)
carcinogen
mutagenesis
Fanconi anemia (FA) pathway
nucleotide excision repair (NER)
prokaryotic (SOS) response

References:

  • Chemistry and biology of DNA damage by malondialdehyde.
    Marnett LJ.
    IARC Sci. Publ., 1999 , :17-27 [PUBMED]

Last modification date: Oct. 3, 2011