Oxidative Balance Flashcards
ROS
reactive oxygen species;
molecular O2, OH-, OH. (radical), superoxide O2-. (1 unpaired and charged)
RNS
reactive nitrogen species; nitric oxide NO. (1 unpaired)
unstable O-O bonds
H2O2 bonds, ONOO-
cell to cell messages via NO
smooth muscle relaxation, vasodilator, neurotrans, hair follicle life cycle;
endothelial cells with NOS release NO and they react with guanylyl cyclase in smooth cells–> vasodilation
NO synthase
L-arginine undergoes reaction with NOS (1,2,or 3) and turns into L-CItrulline + NO.
Uses 2 NADPH
What inhibits NO
Myoglobin
Intracellular ROS
superoxide (made through leaky electrons in the ETC pathway); superoxide dismutase binds the superoxide and binds free radical and makes hydrogen peroxide
hypothesis of superoxide
metabolic state of the cell determines superoxide activity; more ETC activity–> more superoxide; the receptor proteins sense change and the transcriptome/proteome responds
e- in the process of O2 causes
free radicals
enhancing ROS production during ETC
high ETC–> make more ADP, slow down TCA (ADP limiting factor)
diminish ROS production during ETC
uncoupling protein transports H+ into inner membrane without making ATP and ETC is low. Adapt needed–> increase CA cycle;
ROS in inflammation and immunity
NADPH oxidase and arachidonic acid catabolism
NADPH oxidase
in neutorphils;
NADPH redox reaction to NADP which removes e- and reacts with O2 to make superoxide going into phagocytic vesicle or go outside cell;
it’s the first line of defense against infection
how is superoxide used against bacteria?
bacteria are rich in unsequestered Fe2+. Superoxide with protons creates H2O2 which then reacts with Fe2+ via fenton reaction to create more HO. + OH-+ Fe3+
free radicals and metals–> snowball affect
arachidonic acid catabolism
signaling: inflammation and immunity
messengers: nervous system
direct result of autooxidation;
creates leukotrienes and prostanoid eicosanoids
haber-weiss reaction
superoxide and hydrogen peroxide make more hydroxy radical and hydroxy anion and O2 via free iron
ROS attack
bases and backbone of nucleic acids, amino acid side chains, double bonds of unsaturated fatty acids;
non specific
dityrosine bridges
cross linked protein which cannot be degraded via proteosome; created via cysteine, lysine, proline, arginine, metionine cross links
oxidative damage: membrane
via arachidonic acid it creates peroxy cpds, hydroperoxy cpds, OH radical and isoprostanes which lead to rancid membranes
PUFA chain reaction
depletes membrane unsaturated fatty acids; diminished fluidity of membrane
oxidative damage to macromolecules
DNA mutagenesis, protein loss of function, protein aggregation, impaired protein disposal, loss of membrane fluidity, toxic lipid peroxidation byproducts
generalized control of ROS
redundant, enzymatic, nonenzymatic
superoxide dismutase
acts on superoxide
catalse
acts on hydrogen peroxide
glutathione peroxidase/reducase
acts on H2O2;
inactivated by nonspecific glycation in diabetes
thioredoxin enzymes
peroxiredoxin/thioredoxin reductase, variety of substrates
SOD
superoxide dismutase;
takes two superoxides and combines in to hydrogen peroxide
catalase reaction
two hydrogen peroxides to two water and one o2 molecules
non enzymatic antioxidants
tend to be reduced at baseline; accept or donate electrons; become radicals during the process but they are less reactive than neutralized radical because of resonance
drawbacks of antioxidant use
kidney or liver malfunction changes antioxidant metabolism; may interfere with normal signaling or immune response (NADPH oxidase),
why can vitamin c exacerbate kidney stones?
one of the metabolites of vitamin c is oxalate. oxalate is a main component of kidney stones
