reactive oxygen species (ROS)


OTHER NAMES:
oxidative stress


ABBREVIATIONS:
ROS


DESCRIPTION: Reactive oxygen species (ROS) are chemically-reactive molecules containing oxygen. Reactive oxygen species are highly reactive due to the presence of unpaired valence shell electrons. ROS form as a natural byproduct of the normal metabolism of oxygen and have important roles in cell signaling and homeostasis. However, during times of environmental stress (e.g., UV or heat exposure), ROS levels can increase dramatically. This may result in significant damage to cell structures. This cumulates into a situation known as oxidative stress. ROS are also generated by exogenous sources such as ionizing radiation.

In aerobic organisms the energy needed to fuel biological functions is produced in the mitochondria via the electron transport chain. In addition to energy, reactive oxygen species (ROS) that have the potential to cause cellular damage are produced. ROS can damage DNA, RNA, and proteins, which, in theory, contributes to the physiology of ageing.

Of the reactive oxygen species, the highly reactive hydroxyl radical (•OH) reacts with DNA by addition to double bonds of DNA bases and by abstraction of an H atom from the methyl group of thymine and each of the C-H bonds of 2'-deoxyribose. Addition to double bonds of DNA bases occurs at or near diffusion-controlled rates with rate constants from 3 to10 x 109 M-1 s-1; the rate constant of H abstraction amounts to 2 x 10v9 M-1 x s-1. Addition to the C5-C6 double bond of pyrimidines leads to C5-OH and C6-OH adduct radicals and H atom abstraction from thymine results in the allyl radical. Adduct radicals differ in terms of their redox properties, with C5-OH adduct radicals being reducing and C6-OH adduct radicals oxidizing. 

DNA DAMAGES:
Tg from Tg:A
5-formyl dU from 5-formylU:G
8-hydroxyA (8-OH-A)
T:5-OH-U pair
FapyG from FapyG:T
5,6-dihydroxy U (5,6-diOH-U)
5-formyl dU (5-foU)
M1dG
8-oxoG from 8-oxoG:A
FapyG
5-hydroxy-6-hydro-T (5-OH-6-H-T)
5-hydroxy-U (5-OH-U)
5-hydroxymethyl U (5-OH-me-U)
FapyA
8-oxoG
8-oxodGTP
5-OH-meU from 5-OH-meU:A
FapyG from FapyG:C
FapyG from FapyG:G
thymine glycol (Tg)
C:5-OH-U pair
5-OH-meU from 5-OH-meU:G
5-hydroxy-6-hydro-C (5-OH-6-H-C)
5,6-dihydroxy C (5,6-diOH-C)
Tg from Tg:G
2-hydroxy-A (2-OH-A)
2-oxoA from 2-oxoA:G
FapyG:A
5,6-dihydro U (5,6-diH-U)
5-hydroxy C (5-OH-C)
8-oxoG from 8-oxoG:C
A:5-OH-U pair
G:5-OH-U pair
5-hydroxy-6-hydro-U (5-OH-6-H-U)
uracil glycol (Ug)
3,N4-ethenoC (εC) in ssDNA
2-oxoA
8-oxodGDP
Fapy-7meG
8-oxoA
3'-PUA termini
A from A:8-oxoG
5-OH-meU in ssDNA
cytosine glycol (Cg)


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NAME STRUCTURE PROTEINS DNA DAMAGE EFFECT(S) PATHWAY(S) RELATED
Tg from Tg:A NTHL1 stalled replication fork base excision repair (BER)
5-formyl dU from 5-formylU:G MBD4 (MED1) A→G transition
G→A transition
mutagenesis
point mutation
substitution
transition
base excision repair (BER)
heterochromatin formation
8-hydroxyA (8-OH-A) Fpg (MutM)
hOGG1
base excision repair (BER)
T:5-OH-U pair mutagenesis
point mutation
T→A transversion
transversion
FapyG from FapyG:T NTHL1 mutagenesis
point mutation
base excision repair (BER)
5,6-dihydroxy U (5,6-diOH-U) Nth (endo III)
Ung
Nth (endo III)
Nei (endo VIII)
NEIL1
NEIL2
NTHL1
Nth (endo III)
mutagenesis
point mutation
base excision repair (BER)
5-formyl dU (5-foU) Fpg (MutM)
Mug
SMUG1
AlkA
Nth (endo III)
MBD4 (MED1)
NTHL1
Nei (endo VIII)
NTHL1
A→G transition
G→A transition
mutagenesis
point mutation
substitution
transition
base excision repair (BER)
heterochromatin formation
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
8-oxoG from 8-oxoG:A MutY
hOGG1
NEIL2
mutagenesis
point mutation
substitution
base excision repair (BER)
FapyG Fpg (MutM)
hOGG1
NEIL1
NEIL3
NTHL1
mutagenesis base excision repair (BER)
5-hydroxy-6-hydro-T (5-OH-6-H-T) Nth (endo III)
Nei (endo VIII)
NTHL1
mutagenesis
point mutation
base excision repair (BER)
5-hydroxy-U (5-OH-U) Nth (endo III)
Fpg (MutM)
Ung
Mug
Nei (endo VIII)
SMUG1
NEIL1
NEIL2
NTHL1
no mutagenesis base excision repair (BER)
5-hydroxymethyl U (5-OH-me-U) AlkA
Mug
Nth (endo III)
Nei (endo VIII)
TDG
Fpg (MutM)
MBD4 (MED1)
SMUG1
mutagenesis base excision repair (BER)
heterochromatin formation
FapyA Nth (endo III)
Fpg (MutM)
Nth (endo III)
Nei (endo VIII)
NEIL1
mutagenesis base excision repair (BER)
8-oxoG Fpg (MutM)
Nei (endo VIII)
hOGG1
NEIL1
UvrC
UvrB
C→A transversion
G→T transversion
mutagenesis
point mutation
substitution
transversion
base excision repair (BER)
nucleotide excision repair (NER)
prokaryotic (SOS) response
8-oxodGTP MutT modulation of nucleotide pools
5-OH-meU from 5-OH-meU:A SMUG1 mutagenesis base excision repair (BER)
FapyG from FapyG:C hOGG1 mutagenesis
point mutation
stalled replication fork
substitution
base excision repair (BER)
FapyG from FapyG:G NTHL1 mutagenesis
point mutation
base excision repair (BER)
thymine glycol (Tg) Fpg (MutM)
Nei (endo VIII)
NEIL2
NTHL1
Nth (endo III)
C→T transition
mutagenesis
point mutation
stalled replication fork
substitution
T→C transition
transition
base excision repair (BER)
C:5-OH-U pair mutagenesis
point mutation
5-OH-meU from 5-OH-meU:G SMUG1
MBD4 (MED1)
mutagenesis base excision repair (BER)
heterochromatin formation
5-hydroxy-6-hydro-C (5-OH-6-H-C) Nth (endo III) C→T transition
mutagenesis
point mutation
transition
base excision repair (BER)
5,6-dihydroxy C (5,6-diOH-C) Nth (endo III) C→T transition
mutagenesis
base excision repair (BER)
Tg from Tg:G NEIL1
NTHL1
stalled replication fork base excision repair (BER)
2-hydroxy-A (2-OH-A) MUTYH
MutY
mutagenesis
point mutation
base excision repair (BER)
2-oxoA from 2-oxoA:G MutY
MUTYH
mutagenesis
point mutation
substitution
base excision repair (BER)
FapyG:A NTHL1 mutagenesis
point mutation
base excision repair (BER)
5,6-dihydro U (5,6-diH-U) Nei (endo VIII)
NEIL2
Nth (endo III)
mutagenesis base excision repair (BER)
5-hydroxy C (5-OH-C) Nth (endo III)
Fpg (MutM)
Mug
Nei (endo VIII)
NEIL1
NEIL2
NTHL1
C→T transition
transition
base excision repair (BER)
8-oxoG from 8-oxoG:C ANPG (MPG)
hOGG1
NEIL1
NEIL2
no mutagenesis base excision repair (BER)
A:5-OH-U pair no mutagenesis
G:5-OH-U pair G→A transition
mutagenesis
point mutation
transition
5-hydroxy-6-hydro-U (5-OH-6-H-U) Nth (endo III)
Nei (endo VIII)
mutagenesis base excision repair (BER)
uracil glycol (Ug) Nth (endo III)
Fpg (MutM)
Nth (endo III)
Nei (endo VIII)
mutagenesis
stalled replication fork
base excision repair (BER)
3,N4-ethenoC (εC) in ssDNA ALKBH2 C→A transversion
mutagenesis
point mutation
substitution
transversion
direct reversal (DR)
2-oxoA MUTYH
MutY
mutagenesis
point mutation
substitution
base excision repair (BER)
8-oxodGDP MutT modulation of nucleotide pools
Fapy-7meG Fpg (MutM)
hOGG1
NEIL1
NEIL1
base excision repair (BER)
8-oxoA Fpg (MutM)
hOGG1
base excision repair (BER)
3'-PUA termini XthA (exo III)
Nfo (endo IV)
Fpg (MutM)
Nei (endo VIII)
APTX
APEX1
APEX2
cytotoxic
stalled replication fork
nucleotide incision repair (NIR)
base excision repair (BER)
A from A:8-oxoG MUTYH mutagenesis
point mutation
substitution
base excision repair (BER)
5-OH-meU in ssDNA SMUG1
MBD4 (MED1)
mutagenesis base excision repair (BER)
heterochromatin formation
cytosine glycol (Cg) NTHL1 C→T transition
transition
base excision repair (BER)

References:

  • Mitochondrial ROS generation for regulation of autophagic pathways in cancer.

    , , : [PUBMED]
  • Oxidative DNA damage: mechanisms, mutation, and disease.
    Cooke MS., Evans MD., Dizdaroglu M., Lunec J.
    FASEB J., 2003 Jul, 17:1195-214 [PUBMED]

Last modification date: Oct. 3, 2011