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Description : Check out this medical presentation on Alanine Aminotransferase (alanine transaminase), which is titled "AMINO ACID BIOSYNTHESIS", to know about the non-essential amino acids, essential amino acids, single carbon transfers with THF, and physiologic amines.

Tags : Alanine Aminotransferase, alanine transaminase, AMINO ACID BIOSYNTHESIS, single carbon transfers with THF, physiologic amines

Published on : Jul 05, 2021 | Views : 1868 | Downloads : 3

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Slide 1-

AMINO ACID BIOSYNTHESIS NON-ESSENTIAL AMINO ACIDS ESSENTIAL AMINO ACIDS SINGLE CARBON TRANSFERS WITH THF PHYSIOLOGIC AMINES
Slide 2-

AMINO ACID BIOSYNTHESIS “FIXING” OF ATMOSPHERIC N2 DIAZOTROPHS FIX N2 TO NH3 IN MICRO-ORGANISMS, PLANTS, LOWER ANIMALS: GLU DEHYDROGENASE RXN GLU + NAD(P)+ + H2O  -KG + NH3 + NAD(P)H + H+ REVERSE RXN  GLU GLU SYNTHASE RXN’  GLU NADPH + H+ + GLN + -KG  2 GLU + NADP+
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AMINO ACID BIOSYNTHESIS DOES THE GLU DEHYDROGENASE RXN’ WORK IN REVERSE IN MAMMALS? THERE IS SOME CONTROVERSY ABOUT THIS THE HYPERAMMONEMIA/HYPERINSULINEMIA SYNDROME (HI/HA) IS CAUSED BY A MUTATION IN GDH THAT  A GAIN IN FUNCTION SUGGESTS THAT THE PREFERRED DIRECTION IS TOWARD THE RIGHT DEPENDING UPON THE ORGANISM, THE GLU DEHYDROGENASE MIGHT BE CLOSE TO EQUILIBRIUM, OR FAVORED TO THE RIGHT OR LEFT SO, PREFORMED -AMINO NITROGEN, IN THE FORM OF GLU, MUST BE CONSIDERED AN ESSENTIAL NUTRIENT
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AMINO ACID BIOSYNTHESIS ESSENTIAL AMINO ACIDS *ARGININE METHIONINE HISTIDINE PHENYLALANINE ISOLEUCINE THREONINE LEUCINE TRYPTOPHAN LYSINE VALINE NOTE ARG IS ESSENTIAL IN INFANTS AND CHILDREN MOST SYNTHESIZED ARG  ORNITHINE AND UREA VIA THE UREA CYCLE
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AMINO ACID BIOSYNTHESIS NONESSENTIAL AMINO ACIDS ALANINE GLUTAMINE ASPARAGINE GLYCINE ASPARTATE PROLINE *CYSTEINE SERINE GLUTAMATE *TYROSINE NOTE: CYS GETS ITS SULFUR ATOM FROM MET TYR IS HYDROXYLATED PHE SO IT’S NOT REALLY NONESSENTIAL
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AMINO ACID BIOSYNTHESIS ALL ARE SYNTHESIZED FROM COMMON METABOLIC INTERMEDIATES NON-ESSENTIAL TRANSAMINATION OF -KETOACIDS THAT ARE AVAILABLE AS COMMON INTERMEDIATES ESSENTIAL THEIR -KETOACIDS ARE NOT COMMON INTERMEDIATES (ENZYMES NEEDED TO FORM THEM ARE LACKING) SO TRANSAMINATION ISN’T AN OPTION BUT THEY ARE PRESENT IN COMMON PATHWAYS OF MICRO-ORGANISMS AND PLANTS
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AMINO ACID BIOSYNTHESIS OVERVIEW (USE OF COMMON INTERMEDIATES) GLUCOSE  GLUC-6-PHOSPHATE    RIB-5-PHOS→ HIS   3-PHOSPHOGLYCERATE  SERINE    GLYCINE E-4-PHOS + PEP CYSTEINE   PHE→TYR PYRUVATE  ALA TRP  VAL CITRATE LEU, ILE ↓ OXALOACETATE, -KETOGLUTARATE ASP, ASN, GLU, GLN, PRO, ARG, LYS, THR, MET
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SYNTHESIS OF NON-ESSENTIAL AMINO ACIDS ALL (EXCEPT TYR) SYNTHESIZED FROM COMMON INTERMEDIATES SYNTHESIZED IN CELL PYRUVATE OXALOACETATE -KETOGLUTARATE 3-PHOSPHOGLYCERATE
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SYNTHESIS OF NON-ESSENTIAL AMINO ACIDS TRANSAMINATION REACTIONS: ONE STEP PYRUVATE + AA  ALANINE + -KETOACID OXALOACETATE + AA  ASPARTATE + -KETOACID -KETOGLUTARATE + AA  GLUTAMATE + -KETOACID TRANSAMINASES: EQUILIBRATE AMINO GROUPS REQUIRE PYRIDOXAL PHOSPHATE (PLP) ALL AAs, EXCEPT LYS, CAN BE TRANSAMINATED MOST TRANSAMINASES GENERATE GLU OR ASP WHY? LOOK AT MECHANISM OF PLP (PAGE 987 IN TEXT)
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A B C
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SYNTHESIS OF NONESSENTIAL AMINO ACIDS ATP-DEPENDENT AMIDATION OF ASP, GLU  ASN, GLN GLU + ATP + NH3  GLN + ADP + Pi GLUTAMINE SYNTHETASE NH3 IS TOXIC; IT’S STORED AS GLN GLN DONATES AMINO GPS IN MANY REACTIONS ASP + ATP + GLN  ASN + AMP + PPi + GLU ASPARAGINE SYNTHETASE
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SYNTHESIS OF NONESSENTIAL AMINO ACIDS NITROGEN METABOLISM IS CONTROLLED BY REGULATION OF GLUTAMINE SYNTHETASE IN MAMMALS, GLN SYNTHETASES ACTIVATED BY -KG EXCESS AAs TRANSAMINATED TO GLU OXIDATIVE DEAMINATION OF GLU  -KG + NH3 NH3  UREA OR GLN (STORAGE) -KG IS A SIGNAL THAT ACTIVATES GLN SYNTHETASE
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BACTERIAL GLUTAMINE SYNTHETASE VERY DETAILED CONTROL SYSTEM 12 IDENTICAL SUBUNITS (HEX PRISM) ALLOSTERIC CONTROL 9 FEEDBACK INHIBITORS (CUMULATIVE INH) INDIVIDUAL BINDING SITES 6 ARE END-PRODS OF PATHWAYS FROM GLN HIS, TRP, CARBAMOYL PHOSPHATE, AMP, CTP, GLUCOSAMINE-6-PHOSPHATE 3 REFLECT CELL’S N LEVEL (ALA, SER, GLY) ALSO COVALENTLY MODIFIED BY ADENYLYLATION
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BACTERIAL GLUTAMINE SYNTHETASE BRIEF REVIEW: REGULATING ENZYME ACTIVITY NEAR-EQUILIBRIUM (REVERSIBLE) REACTANTS, PRODUCTS ~ EQUIL. VALUES ENZYMES ACT QUICKLY TO RESTORE EQUIL. RATES REGULATED BY [REACT], [PROD] FAR FROM EQUILIBRIUM (IRREVERSIBLE) ENZYME SATURATED NOT ENOUGH ACTIVITY TO ALLOW EQUIL. RATE INSENSITIVE TO [REACT], [PROD]  “STEADY STATE” (CONSTANT FLUX) “RATE-DETERMINING STEP”
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BACTERIAL GLUTAMINE SYNTHETASE BRIEF REVIEW: REGULATING ENZYME ACTIVITY CONTROL OF ENZYME ACTIVITY ALLOSTERIC REGULATION COVALENT MODIFICATION GENETIC CONTROL AT LEVEL OF TRANSCRIPTION
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BACTERIAL GLUTAMINE SYNTHETASE SEE REGULATORY DIAGRAM (PAGE 1035) ADENYLYLATION OF A SPECIFIC TYR RESIDUE  LESS ACTIVITY OF THE ENZYME ENZYME IS ADENYLYLTRANSFERASE IN A COMPLEX WITH A TETRAMERIC REGULATORY PROTEIN, PII URIDYLYLATION OF PII (AT A TYR)  DEADENYLYLATION A URIDYL-REMOVING ENZYME RESULTS IN ADENYLYLTRANSFERASE CATALYZING ADENYLYLATION OF GLN SYNTHETASE
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BACTERIAL GLUTAMINE SYNTHETASE SEE REGULATORY DIAGRAM (PAGE 1035) WHAT CONTROLS ACTIVITY OF URIDYLYL TRANSFERASE? ACTIVATED BY -KG AND ATP DEACTIVATED BY GLN AND Pi URIDYL-REMOVING ENZYME INSENSITIVE TO THESE
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BACTERIAL GLUTAMINE SYNTHETASE IN-CLASS EXERCISE EXPLAIN THE SIGNIFICANCE OF -KG AS AN ACTIVATOR OF GLUTAMINE SYNTHETASE SHOW, IN DETAIL, THE EFFECT OF  LEVEL OF -KG ON THIS ENZYME. DO THE SAME FOR ATP, GLN AND Pi
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NONESSENTIAL AMINO ACID SYNTHESIS PRO, ORNITHINE, ARG ARE DERIVED FROM GLUTAMATE NOTE: 7 OF THE 10 “NONESSENTIALS” ARE ULTIMATELY DERIVED FROM PYR, -KG AND OXALOACETATE SEE PATHWAYS ON PAGE 1036 HIGHLIGHTS: STEP 1: ACTIVATE GLU; A KINASE GLUTAMATE-5-SEMIALDEHYDE BRANCH POINT SPONTANEOUS CYCLIZATION TO AN INTERNAL SCHIFF BASE  PRO TRANSAMINATION TO ORNITHINE  ARG IN UREA CYCLE SCHIFF BASE: AMINE + (ALDEHYDE OR KETONE)  IMINE (CONTAINS A C=N BOND)
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NONESSENTIAL AMINO ACID SYNTHESIS 3-PHOSPHOGLYCERATE IS PRECURSOR OF SER (A 3-STEP PATHWAY) (1) 3-PG + NAD+  3-PHOSPHOHYDROXYPYRUVATE + NADH + H+ (2) 3-PHP + GLU  3-PHOSPHOSERINE + -KG (3) 3-PHOSPHOSERINE + H2O  SER + Pi GLY (2 DIFFERENT WAYS) (1) SER + THF  GLY + N5,N10 – METHYLENE-THF (DIRECT) (2) N5,N10 – METHYLENE-THF + CO2 + NH4+  GLY + THF (CONDENSATION)
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NONESSENTIAL AMINO ACID SYNTHESIS CYSTEINE SER + HOMOCYSTEINE  CYSTATHIONINE HOMOCYSTEINE IS A BREAKDOWN PRODUCT OF METHIONINE CYSTATHIONINE  -KETOBUTYRATE + CYS NOTE: -SH GROUP COMES FROM MET SO CYS IS ACTUALLY AN ESSENTIAL AMINO ACID
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NONESSENTIAL AMINO ACID SYNTHESIS SUMMARY POINT: ALL NONESSENTIALS (EXCEPT TYR) ARE DERIVED FROM ONE OF THE FOLLOWING COMMON INTERMEDIATES: PYRUVATE OXALOACETATE -KG 3-PHOSPHOGLYCERATE
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IN-CLASS EXERCISE WHICH OF THE 4 AMINO ACID INTERMEDIATES OF THE UREA CYCLE IS ESSENTIAL IN CHILDREN? OUTLINE A PATHWAY BY WHICH ADULTS CAN SYNTHESIZE THIS AA FROM 1 GLUCOSE MOLECULE. HINTS: YOU WILL NEED TO CONSIDER THE FOLLOWING METABOLIC PATHWAYS: GLYCOLYTIC GLUCONEOGENIC CITRIC ACID CYCLE GLUTAMATE DEHYDROGENASE REACTION ASSUME IT CAN GO IN REVERSE DIRECTION ORNITHINE PRODUCTION UREA CYCLE
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TRANSFER OF C1 UNITS TO METABOLIC PRECURSORS MOST CARBOXYLATION REACTIONS USE A BIOTIN COFACTOR EXAMPLE: PYRUVATE CARBOXYLASE REACTION S-ADENOSYLMETHIONINE (SAM) AS A METHYLATING AGENT CYTOSINE METHYLATION OF CpGs IN GENE PROMOTER REGIONS TETRAHYDROFOLATES CAN TRANSFER SINGLE C UNITS IN A NUMBER OF DIFFERENT OXIDATION STATES
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TETRAHYDROFOLATES REVIEW STRUCTURE (PAGE 1028 OF TEXT) FOCUS ON HETEROCYCLIC RING STRUCTURE 2-AMINO-4-OXO-6-METHYLPTERIN NOTICE THE NUMBERING OF THE ATOMS LOOK AT N5 PABA JOINS TO 2-AMINO-4-OXO-6-METHYLPTERIN TO FORM PTEROIC ACID FIND N10 COVALENT ATTACHMENT OF C1 UNITS AT N5 N10 BOTH
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TETRAHYDROFOLATE THREE DIFFERENT OXIDATION STATES METHANOL AT N5 METHYL (-CH3) FORMALDEHYDE AT N5,N10 METHYLENE (-CH2-) FORMATE FORMYL (-CH=O) AT N5 OR N10 FORMIMINO (-CH=NH) AT N5 METHENYL ( -CH=) AT N5,N10 LOOK AGAIN AT THE 2 REACTIONS FOR SYNTHESIS OF GLY SERINE HYDROXYMETHYLTRANSFERASE GLYCINE SYNTHASE THF IS INVOLVED IN EACH
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TETRAHYDROFOLATE C1 UNITS ENTER THE THF POOL MAINLY FROM THESE TWO REACTIONS AS N5,N10 –METHYLENE-THF OXIDATION STATES OF C1 UNITS ATTACHED TO THF ARE INTERCONVERTIBLE VIA ENZYMATIC REDOX REACTIONS WE WILL SEE THF AGAIN METHIONINE SYNTHESIS HIS SYNTHESIS PURINE SYNTHESIS dTMP (THYMIDYLATE) SYNTHESIS
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TETRAHYDROFOLATE THF IS DERIVED FROM FOLIC ACID MAMMALS CANNOT SYNTHESIZE IT DEFICIENCY DURING EARLY PREGNANCY CAN LEAD TO NEURAL TUBE DEFECTS ANENCEPHALY   SPINA BIFIDA BACTERIA SYNTHESIZE FOLIC ACID SULFONAMIDES COMPETITIVELY INHIBIT STRUCTURAL ANALOGS OF PABA GOOD ANTIBACTERIAL AGENTS WHY ARE MAMMALS UNAFFECTED?
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TETRAHYDROFOLATE STUDY QUESTION: IF I GIVE YOU THE STRUCTURE OF THF, NUMBERING THE ATOMS ACCORDINGLY, BE ABLE TO SHOW WHERE TO ATTACH THE 5 DIFFERENT C1 GROUPS.
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TRANSAMINATION REACTIONS IN-CLASS STUDY QUESTION DRAW THE STRUCTURES OF THE KETO-ACID PRODUCTS OF THE REACTIONS OF THE FOLLOWING AMINO ACIDS WITH -KG. GLY ARG SER DRAW THE STRUCTURE OF THE AMINO ACID PRODUCT COMMON TO ALL 3 RXNS’
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REFERENCES HERE ARE TWO ARTICLES THAT MIGHT HELP YOU TO ORGANIZE YOUR THINKING ABOUT AMINO ACID METABOLISM: (1) “Glutamate and Glutamine, at the Interface between Amino Acid and Carbohydrate Metabolism” (Brosnan JT, The Journal of Nutrition, Apr 2000, 130,4S: 988S – 990S) (2) “Disorders of Glutamate Metabolism” (Kelly A, Stanley CA, 2001. Mental Retardation and Developmental Disabilities Research Reviews, 7:287-295
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SYNTHESIS OF ESSENTIAL AMINO ACIDS ALL SYNTHESIZED FROM COMMON METABOLIC PRECURSORS ASPARTATE PYRUVATE PHOSPHOENOLPYRUVATE ERYTHROSE-4-PHOSPHATE PURINE + ATP (HISTIDINE) PATHWAYS ONLY IN MICRO-ORGANISMS AND PLANTS PROBABLE EVOLUTIONARY LOSS IN MAMMALS PATHWAYS ARE VERY COMPLICATED ACTUAL PATHWAYS VARY ACROSS SPECIES! IN CONTRAST TO LIPID AND CARBOHYDRATE PATHWAYS, WHICH ARE ALMOST UNIVERSAL
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ESSENTIAL AMINO ACID SYNTHESIS FOUR “FAMILIES” ASPARTATE LYS MET THR PYRUVATE LEU, ILE, VAL (THE “BRANCHED CHAIN” AMINO ACIDS) AROMATIC PHE TYR TRP HISTIDINE
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THE ASPARTATE FAMILY FIRST COMMITTED STEP IS ASP + ATP  ASPARTYL-β-PHOSPHATE + ADP ENZYME: ASPARTOKINASE 3 ISOZYMES IN E.coli EACH RESPONDS DIFFERENTLY AS FAR AS FEEDBACK INHIBITION AND REPRESSION OF ENZYME SYNTHESIS THR,LYS, MET PATHWAYS INDEPENDENTLY CONTROLLED
Slide 38-

THE ASPARTATE FAMILY CONTROL OF ASPARTOKINASE ISOENZYMES ENZYME FEEDBACK INHIB COREPRESSOR ASP I THR THR, ILE ASP II NONE MET ASP III LYS LYS COREPRESSOR: TRANSCRIPTIONAL REPRESSION
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ASPARTATE FAMILY ALSO CONTROL AT BRANCH POINTS NOTE THE FOLLOWING REACTION: HOMOCYSTEINE + N5-METHYL-THF  MET + THF ENZYME: METHIONINE SYNTHASE (?)  HOMOCYSTEINE  CV DISEASE RISK FACTOR EAT FOODS CONTAINING FOLATE RECALL:SER + HOMOCYSTEINE  CYSTATHIONINE ENZYME DEFECTS IN REMETHYLATION OF HOMOCYSTEINE TO MET OR IN RXN’ FROM CYSTATHIONINE  CYS   HOMOCYSTEINE DEFECT IN SYNTHESIS OF CYSTATHIONE-β-SYNTHASE HYPER HOMOCYSTENEMIA  HOMOCYSTEINURIA SYMPTOMS: PREMATURE ATHEROSCLEROSIS THROMBOEMBOLIC COMPLICATIONS SKELETAL ABNORMALITIES ECTOPIA LENTIS MENTAL RETARDATION
Slide 40-

THE PYRUVATE FAMILY “BRANCHED CHAIN AMINO ACIDS” LEU ILE VAL VAL, ILE: SAME PATHWAY AFTER 1st STEP LEU PATHWAY BRANCHES FROM VAL PATHWAY FINAL STEPS ALL CATALYZED BY AMINO- TRANSFERASES GLU IS THE AMINO DONOR
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THE PYRUVATE FAMILY THE FIRST STEP: PYR + TPP  HYDROXYETHYL-TPP FIRST PYR AND TPP FORM AN ADDUCT THEN DECARBOXYLATED TO HE-TPP A RESONANCE-STABILIZED CARBANION A STRONG NUCLEOPHILE ADDS TO KETO GROUP OF PYRUVATE  VAL, LEU -KETOBUTYRATE  ILE
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THE PYRUVATE FAMILY LOOK AT THE REACTION MECHANISM OF PYRUVATE DECARBOXYLASE (PAGE 605) THIS SHOWS THE FORMATION OF THE HYDROXYETHYL-TPP ADDUCT THIAMINE (VIT B1) SOME INTERESTING CHEMISTRY THIAZOLIUM RING ACIDIC HYDROGEN “ELECTRON SINK” TRANSITION STATE STABILIZATION MECH. YLIDS RESONANCE
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THE AROMATIC FAMILY IN PLANTS AND MICRORGANISMS PHE TYR TRP PECURSORS ARE: PEP ERYTHROSE-4-PHOSPHATE THESE CONDENSE WITH ULTIMATE CONVERSION TO CHORISMATE
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THE AROMATIC FAMILY CHORISMATE BRANCH POINT FOR TRP SYNTHESIS CHORISMATE ANTHRANILATE TRP CHORISMATE  PREPHENATE PREPHENATE BRANCH POINT FOR PHE, TYR SYNTH AMINOTRANSFERASES IN EACH FINAL STEP IN MAMMALS, TYR IS A PRODUCT OF: PHE HYDROXYLATION
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THE TRP PATHWAY TRYPTOPHAN SYNTHASE CATALYZES FINAL 2 STEPS INDOLE-3-GLYCEROL PHOS  INDOLE + GLYC-3-P INDOLE + SER  H2O + TRP 2β2 BIFUNCTIONAL ENZYME WHAT ENZYME CLASS?
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THE TRP PATHWAY “CHANNELING” INDOLE IS SEQUESTERED BETWEEN THE TWO ACTIVE SITES DIFFUSES BETWEEN TWO SITES IT’S NONPOLAR STUDY QUESTION: WHAT ARE THE BENEFITS OF CHANNELING? SEE RIBBON DIAGRAM OF TRP SYNTHASE ON PAGE 1044 MECHANISM?
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PHENYLKETONURIA (PKU) DEFECTIVE OR ABSENT PHENYLALANINE HYDROXYLASE CANNOT FORM TYROSINE PHE BUILDS UP  PHE IS TRANSAMINATED TO PHENYL-PYRUVATE SEVERE MR IF NOT TREATED SOON AFTER BIRTH WITH LOW PHE DIET UNIVERSAL NEWBORN SCREENING
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PHENYLKETONURIA IN-CLASS STUDY QUESTION WRITE OUT THE REACTION IN WHICH PHE IS TRANSAMINATED TO PHENYLPYRUVATE, SHOWING STRUCTURES EXPLAIN WHY CHILDREN WITH A TETRAHYDRO-BIOPTERIN DEFICIENCY EXCRETE LARGE AMOUNTS OF PHE WHY DO PEOPLE WITH PKU HAVE BLOND HAIR, BLUE EYES AND VERY LIGHT SKIN? WHY DO PEOPLE ON A LOW PHE-DIET NEED TO INCREASE THEIR TYR INTAKE?
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HISTIDINE BIOSYNTHESIS ATOMS DERIVED FROM: 5-PHOSPHORIBOSYL--PYROPHOSPHATE PROVIDES 5 C-ATOMS PRPP INVOLVED IN PURINE SYNTHESIS PRPP INVOLVED IN PYRIMIDINE SYNTHESIS PURINE SALVAGE PATHWAY AN INTERMEDIATE IN TRP SYNTHESIS ATP PROVIDES THE 6th C-ATOM ATP + -D-RIBOSE-5-PHOSPHATE  PRPP + AMP -D-RIBOSE-5-PHOSPHATE FROM H-M SHUNT
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HISTIDINE BIOSYNTHESIS NOTICE THE PRODUCTS OF THE AMIDO-TRANSFERASE STEP: AICAR AN INTERMEDIATE IN PURINE BIOSYNTHESIS IMIDAZOLE GLYCEROL PHOSPHATE THERE IS AN APPARENT EVOLUTIONARY OVERLAP OF PURINE AND HIS SYNTHESIS THE FIRST STEP IN HIS SYNTHESIS INVOLVES FORMATION OF A PURINE!
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HISTIDINE BIOSYNTHESIS IS THE HIS PATHWAY A RELIC OF THE TRANSITION FROM RNA-BASED TO PROTEIN-BASED LIFE FORMS? HIS IS FREQUENTLY FOUND IN ENZYME ACTIVE SITES NUCLEOPHILES GENERAL ACID/BASE CATALYSIS RNA HAS CATALYTIC PROPERTIES IMIDAZOLE GROUP PROBABLY PLAYS A SIMILAR ROLE
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PHYSIOLOGICALLY ACTIVE AMINES THESE ARE DERIVED FROM AMINO ACIDS THEY INCLUDE EPINEPHRINE (ADRENALINE) NOREPINEPHRINE DOPAMINE SEROTONIN -AMINOBUTYRIC ACID (GABA) HORMONES NEUROTRANSMITTERS
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PHYSIOLOGICALLY ACTIVE AMINES DECARBOXYLATION OF PRECURSOR AMINO ACID PLP-DEPENDENT, AA DECARBOXYLASES TYR  DOPAMINE, EPI, NOREPINEPHRINE GLUTAMATE  GABA HISTIDINE  HISTAMINE TRP  SEROTONIN
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DECARBOXYLATION REACTION PLP FORMS A SCHIFF BASE WITH AA RESULTS IN FORMATION OF C CARBANION UNSTABLE CHARGE BUILDUP ON C WHEN CO2 SPLITS OFF PLP IS AN “ELECTRON SINK” IN-CLASS EXERCISE: USING THE STRUCTURE OF THE AMINO-ACID-PLP SCHIFF BASE AS SHOWN IN CLASS, SHOW (USING ARROWS TO SHOW FLOW OF ELECTRONS) HOW THE C CARBANION FORMED AFTER CO2 SPLITS OFF IS STABILIZED.
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GABA GLUTAMATE  GABA + CO2 GLU DECARBOXYLASE GABA IS THE MAJOR INHIBITORY NEURO-TRANSMITTER IN BRAIN GLU IS THE MAJOR EXCITATORY NEURO-TRANSMITTER STIMULATION OF NEURONS BY GABA   PERMEABILITY TO CHLORIDE IONS BENZODIAZEPINES (VALIUM) ENHANCE MEMBRANE PERMEABILITY OF Cl IONS BY GABA GABAPENTIN PROTECTS AGAINST GLU EXCITOTOXICITY
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HISTAMINE HISTIDINE  HISTAMINE + CO2 HIS DECARBOXYLASE HISTAMINES INVOLVED IN ALLERGIC RESPONSE H1 RECEPTORS IN GUT, BRONCHI STIMULATION  SMOOTH MUSCLE CONTRN’ H1 RECEPTOR ANTAGONISTS CLARITIN, ZYRTEC, ETC
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HISTAMINE HISTAMINES INVOLVED IN CONTROL OF ACID SECRETION IN STOMACH H2 RECEPTORS STIMULATION   HCl SECRETION H2 ANTAGONISTS CIMETIDINE RANITIDINE H2 RECEPTORS IN HEART STIMULATION   HEART RATE
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SEROTONIN TRP  5-HYDROXYTRYPTOPHAN TRP HYDROXYLASE REQUIRES 5,6,7,8 TETRAHYDROBIOPTERIN 5-HT  SEROTONIN + CO2 AROMATIC ACID DECARBOXYLASE SEROTONIN CAUSES SMOOTH MUSCLE CONTRACTION BRAIN NEUROTRANSMITTER MELATONIN SYNTHESIZED IN PINEAL GLAND
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CATECHOLAMINES EPI, NOREPINEPHRINE, DOPAMINE AMINE DERIVATIVES OF CATECHOL REACTIONS: TYR  L- DOPA TYR HYDROXYLASE L-DOPA  DOPAMINE + CO2 AROMATIC ACID DECARBOXYLASE DOPAMINE  NOREPINEPHRINE DOPAMINE β-HYDROXYLASE NOREPINEPHRINE  EPINEPHRINE REQUIRES SAM
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L-DOPA AND DOPAMINE IN SUBSTANTIA NIGRA, CATECHOLAMINE PRODUCTION STOPS AT DOPAMINE PARKINSON’S DISEASE: DEGENERATION OF SUBSTANTIA NIGRA   DOPAMINE TREAT BY GIVING PRECURSOR, L-DOPA DOPAMINE CANNOT CROSS BLOOD/BRAIN BARRIER TRANSPLANTATION OF ADR. MEDULLA CELLS TO BRAIN L-DOPA A PRECURSOR OF MELANIN PRODUCTION
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IN-CLASS EXERCISE IN KWASHIORKOR, A DIETARY PROTEIN DEFICIENCY DISEASE IN CHILDREN, DEPIGMENTATION OF HAIR AND SKIN IS SEEN. EXPLAIN THE BIOCHEMICAL BASIS FOR THIS.
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S-ADENOSYLMETHIONINE
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ACTIONS OF NOREPINEPHRINE NOT NEARLY AS ACTIVE AS EPINEPHRINE DURING EXTREME STRESS CIRCULATORY SYSTEM CONSTRICTS GREAT VEINS (2) VASOCONSTRICTIVE TO SKIN (1) VASOCONSTRICTION (1) EFFECTS ON GI TRACT SPLEEN PANCREAS KIDNEYS NEUROTRANSMITTER IN THE BRAIN
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ACTIONS OF EPINEPHRINE AS AN INSULIN ANTAGONIST ACTIVATES MUSCLE GLYCOGEN PHOSPHORYLASE GLUCOSE-6-P USED IN GLYCOLYSIS TRIGGERS PHOSPHORYLATION (ACTIVATION) OF HORMONE-SENSITIVE LIPASE IN FAT CELLS MOBILIZES FAT BY HYDROLYZING TGs GLYCOGEN BREAKDOWN IN LIVER ACTIVATES GLUCONEOGENESIS IN LIVER INHIBITS FATTY ACID SYNTHESIS
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ACTIONS OF EPINEPHRINE ON CARDIAC MUSCLE β1 -ADRENERGIC RECEPTOR STIMULATION  HEART RATE AND CARDIAC OUTPUT β-BLOCKERS   BLOOD PRESSURE DILATES CORONARY ARTERIES (β2) ON SMOOTH MUSCLE (β2-ADRENERGIC) IN BRONCHIOLES, FOR EXAMPLE  MUSCLE RELAXATION ACTIVATION OF G-PROTEINS cAMP , ETC ASTHMA MEDICATIONS
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AMINO ACID METABOLISM SUMMARY 1 SYNTHESIS ESSENTIAL ASPARTATE FAMILY PYRUVATE FAMILY AROMATIC HISTIDINE NON-ESSENTIAL PYRUVATE OXALOACETATE -KETOGLUTARATE 3-PHOSPHOGLYCERATE
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AMINO ACID METABOLISM SUMMARY 2 DEGRADATION TO: PYRUVATE ACETYL-CoA ACETOACETATE -KETOGLUTARATE SUCCINYL-CoA FUMARATE OXALOACETATE
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AMINO ACID METABOLISM SUMMARY 3 KETOGENIC LEU LYS GLUCOGENIC ALL NON-ESSENTIALS + HIS, VAL,MET BOTH ILE PHE THR TRP TYR
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IN-CLASS STUDY QUESTION EXPLAIN WHY IT IS POSSIBLE FOR THE CARBON SKELETON OF EACH AMINO ACID TO BE BROKEN DOWN TO ACETYL-CoA.
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AMINO ACID DEGRADATION INTERMEDIATES CO2 CO2