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FSHN 470- Unit 3

3 common ROS superoxide (O2-), hydroxyl OH-, perhydroxyl OOH-
5 sources of radicals activated macrophages, NO synthase, ionizing radiation, transition metals + oxygen, oxidation of reduced flavins
ROS chain reaction R- created from OH-, then another one is made at end and reaction repeats
PUFA oxidation very stable b/c of resonance stabilization
why don't radicals form on saturated or monounsaturated? unstable & revert back to starting product
why is lipid peroxidation of membranes bad? -OOH push bilayer apart & makes them leaky (ions get back in)
LDL oxidation apo B100 + charges go away, then must be picked up my macrophages instead of binding to receptor
oxyradicals and cancer OH- and ROO- activate many signaling pathways involved in gene expression/cell growth
SOD is __ dependent Cu and Mn
cytoplasmic SOD Cu dependent, and Zn structural role
extracellular SOD Cu dependent
mitochondrial SOD Mn-dependent, functions and expressed only in the mitochondria
ferric iron Fe3+
ferrous iron Fe2+
glutathione tripeptide in all cells in high conc; (glutamate, cysteine, glycine) *abbreviated as GSH (SH provides reducing equivalents)
glutatione peroxidases quenches H2O2 and FFA hydroperoxides
three types of GSHPx cytoplasmic (H2O2/FFA hydroperoxides), plasma, phospholipids
GSHPx's are different in ___, but same in that ___ they come from different genes (distinct enzymes), they require Se as a cofactor
where is Selenium toxicity seen? American west from locoweeds
where does regeneration of vitamin E occur? interface of aqueous and lipid portion of cells (due to different solubilities)
why should you not take excess vitamin C? it's a pro-oxidant in excess
how does vitamin C help protect LDL from oxidation? re-generates vitamin E, which intercepts radicals of LDL
phytonutrients many are antioxidants and intercept free radicals similar to how vitamin E functions
what are the 4 human desaturases? Δ9, Δ6, Δ5, Δ4
regulation of desaturases & elongases NO PHOSPHORYLATION, response element (when fed)
which desaturase is the most responsive to fasting/feeding? Δ9
2 essential fatty acids linoleic & a-linolenic
does n-6 consumption affect tissue arachidonic acid? no, plateaus at 2-3% of kcal
what is made if n3 is deficient? DPA
what is made if both n3 and n6 are deficient? mead acid (Δ6 desaturated, 2C elongation, Δ5 desaturation of oleic acid)
major product of n-3 FAs DHA (very little EPA), but only 1% conversion from n-3 to these
regulation of n-3/n-6 pathways by insulin increases expression of Δ6 and Δ5
which step in n-3/n-6 pathway is limiting? Δ6 desaturase (1st step)
how can Δ6 and Δ5 desaturases be down-regulated? high PUFA in the diet
US ratio of n-6/n-3 10:1 (4:1 before increased use of vegetable oils in 1950s)
optimal ratio n-6/n-3 (paleonutritionists) 2:1 or 3:1
major source of DHA in Americans chicken
does diet linolenic acid affect phospholipid DHA? not significantly- must eat EPA and DHA (they also decrease phospholipid AA)
are people deficient for n-3? no, health conditions just improve with increased intake of them!
linoleic acid AI ~15g *no AI for AA b/c not essential
linolenic acid AI ~1.5g *no AI for EPA/DHA b/c not essential
eicosanoids produced where? locally (paracrine)- mostly from AA
what do eicosanoids do? normal & inflammatory states
arachidonic acid gives rise to group 2 prostanoids, leukotrienes, and lipoxins
linoleic acid gives rise to group 1 prostanoids and leukotrienes
a-linolenic acid gives rise to group 3 prostanoids and leukotrienes
cyclooxygenase makes __ prostanoids and thromboxanes
lipoxygenase makes ___ leukotrienes and lipoxins
what is the common intermediate for all prostaglanins? PGH2
PGH synthase (aka COX); 2 domains; COX (adds 2 O2), peroxidase (reduces PGG2 to PGH2)
half-lives of PGs degrades in seconds or quickly degraded by kidney/lung enzymes
COX-1 isoform of PGHS constitutive isozyme; always present; expressed in all cells (housekeeping fxns)
COX-2 isoform of PGHS inducible isozyme, inflammatory signals
EPA dietary effects PGHS has low affinity for EPA; so enriches phospholipid EPA & displaces PL AA; small increase in 3-series PG
DHA dietary effects only effect is to displace AA from PLs
TXA2 platelet PG (atherogenic)
PGI2 endothelial cell PG (anti-atherogenic) *counters TXA2
GI cancer and PG colon cancer proliferates by PGE2-dependent processes, if block COX2, blocks colon cancer
osteoarthritis PG inflammatory cytokines -> COX2 production of PGE2-> collagen degradation->osteoarthritis
regulation of COX2 n-3 PUFA block expression of COX2 via SREBP
NSAIDs inhibit both cox1 and cox2
first NSAID acetylsalicylic acid (aspirin)
how does aspirin work? acetylates COX1 at a serine (inhibits it), stops COX2 activity (no PGH2 made), acetylated COX2 produces signaling molecules from EPA/DHA
acetaminophen doesn't relieve inflammation, but few side effects
ketoprofen/naproxen 8 hour pain relief (NSAID)
voltaren arthritis- more specific for COX2- fewer GI problems
COX2 inhibitor problems excess CVD deaths from these
COX2 CVD does nothing to TXA2 (which is prothrombic) decreases PGI2 (which is a vasodilator)
low dose aspirin enough to decrease TXA2, but not enough to decrease PGI2 (significantly)
SCOT (ketolytic tissues) converts acetoacetate to acetoacetyl-coA
2 regulatory enzymes in ketone metabolism SCOT and HMGCS2
HMGCS2 regulation activated by glucagon, inhibited by insulin and succinyl co-A
SCOT regulation inhibited by insulin and transcription factors
ketogenesis helps with what? prevents accumulation of incompletely oxidized FA intermediates, provides energy substrates in glucose-limited states in low CHO high FA conditions
how does liver switch to produce ketone bodies? less OAA b/c of gluconeogenesis, so can't use TCA; FFA inhibits pyruvate kinase and acetyl coA in mitochondria inhibits pyruvate dehydrogenase
is ketone body regulation increased by FFA coming to liver? no- KB would increase from exercise/stress which does not occur
NADH and ketones as NADH increases, so does beta hydroxy butyrate, which goes to blood; if NADH drops, acetoacetate goes up, which will be converted to acetoacetyl coA and shut down KB production
what enzyme(s) transfer NH2 group to another alpha-keto acid? aminotransferases
what enzyme converts NH2 to NH3? glutamate dehydrogenase
which 3 amino acids cannot be transaminated? lysine, threonine, and proline
which vitamin activates transaminases? B6 (pyridoxine)
what is the only ketogenic amino acid? leucine
what makes an amino acid glycogenic? 3 or more carbons for gluconeogenesis
how many ATPs are needed to break down 1 NH4? 4, but NADH is made so only 1
carbamoyl phosphate synthase 1 regulation (1st enzyme of urea cycle- in gut) n-acetyl glutamate (from glutamate)= positive allosteric effector
ornithine transcarbamoylase (2nd enzyme of urea cycle- in gut) ornithine controls flux
long term urea enzyme regulation (ornithine transcarbamoylase) 5x increase after 4-8 days; mechanism is probably transcription or translation
60% of AA in muscle are alanine and glutamine
most nitrogen into urea cycle can also come from (& what enzyme?) purine metabolism; AMP deaminase
only __ has all 5 urea cycle enzymes liver (gut has ornithine transcarbamoylase and carbamoyl phosphate synthase)
feasting: increased ornithine in the liver does what? increases flux through urea cycle via Km effects
gut is the key to urea cycle why? citruline from gut increases liver ornithine, increased flus thru urea cycle
pentose phosphate ribose 5- phosphate -> nucleotides + NADPH
alanine's alpha keto acid pyruvate
aspartate's alpha keto acid oxaloacetate
glutamine is used as an energy substrate
branched chain AA use fat storage, nitrogen
aromatic AA use tryptophan converted to serotonin in the brain
glucose & ketone use starvation day 3 vs 30 3: 2x as much glucose as ketones; 30: 2x as many ketones as glucose
adipose & muscle use starvation day 3 vs 30 3: 2-3x adipose as muscle 30: 9x adipose as muscle *amt of adipose doesn't change, muscle just goes down
fuel output of liver starvation day 3 vs 30 3: 1:1 ratio glucose and ketones 30: 2x ketones than glucose
other effects of trauma (2 hormones) water retention from ADH; sodium retention from aldosterone
how is BAT different than WAT? (4) high lipid content, small lipid droplets, more vascularized, more mitochondria
protein that permits H+ flux w/out ATP production thermogenin aka UCP
higher BAT in which gender? women
mass of BAT correlates inversely with BMI
what mineral is required for T3 and T4 in BAT? iodine
sleeping BAT study 19C (66F)-> higher DIT and insulin sensitivity (reversible w/ higher temps)
white adipose comes from (2) endothelial precursor or WAT precursor
brown adipose comes from (2) muscle satellite cell or BAT precursor
difference b/w beige and brown adipocytes beige come form white; BAT different origin
which eicosanoid is involved in osteoarthritis and colon cancer? PGE2
HMGCS1 vs HMGCS2 1: HMG Co-A for cholesterol synthesis 2: HMG Co-A for acetoacetate
Created by: melaniebeale



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