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61 Cards in this Set

  • Front
  • Back

Alanine Aminotransferase (ALT)

Viral hepatitis

Aspartate aminotransferase (AST)

alcoholic hepatitis,


MI



Alkaline phosphatase

Osteoblastic bone disease

Amylase

acute pancreatitis, mumps

Creatine Kinase

MU


Duchenne muscular dystrophy

y-Glutamyl transferase (GGT)

obstructive liver disease, (high in alcoholics)

LActate dehydrogenase (LDH, type I)

MI

Lipase

Acute pancreatitis

ΔG -ve

net loss of energy




Reaction will go spontaneously




Reaction is EXERGONIC

ΔG +ve

net gain of energy




Reaction will not go spontaneously




Reaction is ENDERGONIC




Energy must be supplied to make reaction go

ΔG°´ provides

(i) a uniform convention for measuring free energy changes




(ii) a definition of where the equilibrium lies

ATP-->ADP + Pi

ΔG°´ = -7.3 kcal/mol

ADP->AMP + Pi

ΔG°´ = -7.3 kcal/mol

AMP-->A + Pi

ΔG°´ = -3.4 kcal/mol

Endergonic Vs Exergonic

The ‘business end’ of NAD+is made from

vitamin B3


Niacin

Niacin deficiency causes

pellegra, 3 Ds




Dementia, diahrrea,

Most of our ATP is produced by

oxidative phosphorylation, except in hypoxic circumstances

absence of an adequate oxygen supply

ATP is produced by anaerobic glycolysis

glycolysis biosynthetic roles

Fatty acid biosynthesis
Triacyl glycerol
Amino acid
Ribose-5-P
2,3 bisphosphoglycerate (for Hb fx)


23FATR

TCA

operates aerobically, only happens in mitochondrion, major source of ATP,

Acetyl CoA made from

FA, ketone bodies, Glucose, Acetate, AA, alcohol



Lipoic acid

a COENZYME not a vitamin

Wet beri-beri

edema (heart failure)

Dry beri-beri

polyneuropathy

ALCOHOL impairs

THIAMINE ABSORPTION


Consequently Beri-beri is often seen in chronic alcoholics

Succinate thiokinase
Substrate-level phosphorylation

succinate DEHYDROGEASE

Embedded in inner mitochondrial membrane

thiamine (vit B) deficiency causes issues with

pyruvate dehydrogenase

produce NADH and CO2 in TCA cycle

Isocitrate, alpha ketoglutarate

1 turn of TCA cycle makes

10 ATP

citrate makes

Fatty acids happens in cytoplasm

aplha- ketoglutarate

makes AA and GABA

succinyl CoA

makes heme

Malate

starting point for gluconeogenesis

Oxalacetate

AA synthesis

Pyruvate carboxylase

replenishes oxaloacetate (NEEDS biotin)




activated by pyruvate carboxylase



Alpha-ketoglutarate

made from glutamate (AA)

Odd # FA

make succinyl CoA

biotin can be taken up by

avidin (in egg protein)

Pyruvate dehydrogenase complex

does pyruvate to acetyl CoA




inhibited by NADH, and acetyl CoA




pyruvate dehydrogenase: inactive by phosphorylation (kinase activated by NADH and acetyl CoA, deactivated by ADP and pyruvate)




pyruvate dehydrogenase: activated by Ca ions




Needs:


Thiamine, pyrophosphate, Lipoate, FAD

Pyruvate dehydrogenase activators

Pyruvate


CoA


NAD+


Ca++


ADP

Pyruvate dehydrogenase inhibited by

NADH and Acetyl CoA

TOM

Translocases of the outer membraneof mitochondria

TIM

Translocases of the inner membrane of the mitochondria

TIM/TOM

THE OUTER 'MATRIX PROTEIN' SHOULD BE CYTOPLASMIC PROTEIN

THE OUTER 'MATRIX PROTEIN' SHOULD BE CYTOPLASMIC PROTEIN

The “hydrogen acceptor” part of NAD+ is made from

niacin (vitamin B3)

The electron transport chain is located in

the inner mitochondrial membrane

succinate dehydrogenase complex

Complex II embedded within the membrane

One complete turn of the rotor of ATP synthase enzyme make/needs

3 ATP and needs 12 protons

Niacin (vitamin B3) deficient

Complex I

Riboflavin (vitamin B2) deficient

Complex II

Fe (for heme synthesis) deficient

Complex III


Cytochrome c


Complex IV

dinitrophenyol

causes decoupling of the proton gradient from ATP production

Thermogenin

protein that moves H across membrane and creates heat instead of ATP in Brown Fat

Asprin

Blood [lactate] increase causing metabolic acidosis




ATP decrease, AMP increase, stimulating glycolysis

Mt DNA encodes (mitochondrial DNA)

encodes rRNA, tRNA and proteins involved in oxidative phosphorylation

LHON (Leber’s Hereditary Optic Neuropathy)

Sudden blindness in young males




Less common symptoms – mild dementia, ataxia, peripheral neuropathy.




Inherited maternally




Caused by various mutations in complexes I, II and IV polypeptides encoded by mitochondrial DNA




90% caused by mutations in NADH dehydrogenase

MERRF (Myotonic Epilepsy and Ragged Red Fiber Disease)

Myoclonus, ataxia, muscle weakness, deafness and progressive dementiaCaused by mutations in mitochondrial RNAs (most commonly mtRNA-lys

MELAS (Mitochondrial Myopathy, Encephalomyopathy, Lactic Acidosis and Stroke-like episodes)

Progressive neurodegenerative disease – onset at 5 -15 years.Caused by mutations in tRNA-leu

intracellular signaling molecule:


2nd messengers

small molecules that increase in concentration when a ligand binds:


Diacyl glycerol, IP3, Ca, cAMP, cGMP)