1. dia

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Nomenclature of Enzymes
Classes on the basis of reaction type and
functional groups.For enzyme classes and
subclasses arabic numbers are used. Oxidoreductase
NAD(P) acceptor 1.1.1.1 CH-OH
donor alkohol-dehydrogenase
Main enzyme classes 1. Oxidoreductase 2.
Transferase 3. Hydrolase 4. Lyase 5.
Isomerase 6. Ligase
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Main class kind of reaction Sub-class donor
group or the type of the reaction Sub-sub-class
acceptor group or substrate Serial number
specifies the enzyme itself e.g. 1.2.3.4 means
oxidoreductases aldehyde group donor oxygen
acceptor oxalate oxidase Main classes 1.
oxidoreductases 2. transferases 3.
hydrolases 4. lyases 5. isomerases 6.
ligases
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1.) Oxidoreductases 1.X.1.Y NAD or NADP
acceptors dehydrogenases 1.6.4.Y. NADPH
H-donor (and S-S H-acceptor) reductases 1.3.X.Y
.O2 electron acceptor, H2O2 product
oxidases (except cytocrhome-oxidase
H2O) Monooxygenases 1 atom oxygen built in,
another forms water Dioxygenases both oxygen
atoms built in Peroxidases H2O2 or R-OOH
degradation Coenzymes of oxidoreductases may
be NAD, NADP, FAD, FMN, lipoate, ascorbate, DHB,
cytochromes, iron-sulfur centres
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2.) Transferases 2.1.1. methyltransf. coenzyme
SAM S-adenosylmethionine (exceptionally
betain, methyl-THF) 2.1.2. C-1 units methyl-,
hydroximethyl-, formyl-, formimino-,
methylene-, methenyl- coenzyme THF
tetrahydrofolate 2.2. ketogroup transketolase
TPP, transaldolase 2.3.1. acyltransf. coenzyme
HS-CoA coenzyme A 2.4. glycosyltransferases.
di-, oligo- and polysaccharide formation
(synthases) active forms UDP-sugar
(UDP-glucuronate, PRPP) 2.6.1. aminotransferases
amino acid1 oxo acid2 oxo acid1 amino
acid2
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2.7. Phosphotransferases kinases donor
ATP acceptor OH-, COO--, NH2-, HPO42-, etc.
2.8.2. Sulfotr. sulphate transfer coenzyme
PAPS (phosphoadenosyl-phosphosulfate) 3.)
Hydrolases (hydrolysing enzymes) 3.1.
esterases carboxyl-, thiol-, phosphate-,
sulphate ester hydrolysing 3.2. glycosidases
oligo- és polysaccharide cleaving 3.4.
peptidases, proteases protein degrading 4.)
Lyases addition to double bonds or small
molecule elimination 4.1. 1.decarboxylases,
coenzyme PLP 4.1.3. oxo acid lyases
citrate-synthase or lyase
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4.2.1. Hydrolyases water elimination or
addition fumarase, enolase, akonitase 4.6.1.1.
adenylate-cyclase 5.) Isomerases 5.1. Racemases
and epimerases one group position changed 5.2.
cis-trans isomerases 5.3.1. aldo-keto isomerases
(aldose-ketose) 5.3.3. double bond position
changers (unsaturated fatty acids) 6.) Ligases
synthetases ATP, CTP, GTP requiring 6.1.1.
aminoacyl-tRNA synthetases 6.2.1.acyl-CoA
synthetases 6.3.2. peptid synthetases e.g.
glutathione GSH 6.3.5.acid amide producing with
Gln donor (GMP, Asn) 6.4. carboxylases, coenzyme
biotin
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• Vitamins obligatory need for the living
  organisms for the life - the given creature can
  not produce, it has to eat
• take part in enzyme catalysis, or they are
  hormons or
• other regulating factors.
• small organic molecules
• B-vitamins 1,2,3,5,6,7,9,12 and vitamin C
  are water soluble
• A,D,E,K vitamins are lipid soluble
• Coenzyme loosely bound, easily dissotiated from
  the enzyme, taking part in catalysis, small
  organic molecule NAD, NADP, CoA
• Prosthetic group strictly bound to enzymes, not
  dissociated, taking part in catalysis, small
  organic molecule FAD, FMN, TPP, PLP, THF, DHB,
  biotin, cobalamine

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Effect of alcoholism on the metabolism of
vitamins 1.) gastroenteritis, diarrhoea ? wrong
absorption 2.) steatohepatitis, cirrhosis ?
storing capacity of the liver is
decreased especially pyridoxal, folate,
cobalamin 3.) competition with acetaldehyde on
transport protein ? pyridoxin degradation is
increased 4.) iron absorbtion increased ? iron
deposits in liver, ROS formation
Coenzymes of energy producing pathways NAD, FAD,
FMN, TPP, CoA, (PLP), biotin Any of them is
missing ? carbohydrate- lipid-, amino acid
degradation is decreased ? ATP shortage ? fast
multiplicating cells (intestine, skin, blood
cells) and big energy requireing organs (nervous
system, heart, muscles) can not work properly
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Vitamins taking part in amino acid and nucleotid
metabolism pyridoxin, folate, cobalamin In
their deficiency the metabolism of amino acids
and synthesis of nucleotides, therefore synthesis
of nucleic acids (DNA, RNA) is improper mainly
in fast replicating cells blood cells,
enterocytes, skin, mucous membranes
Excess water soluble vitamins are excreted by
kidney, some of them are stored in liver folate,
cobalamin (6 years), pyridoxin (2 month). Even
pharmacological doses do not cause poisoning or
overdosage, except vit. B3 and B6. Lipid
soluble vitamins absorbed and transported
together with lipids. Pharmacological doses
cause poisoning of vitamin A or D. Vitamin E
has many adventageous characteristics, no
overdosing
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Vitamin B1 tiamin ? TPP thiamin-pyrophosphate
prosthetic group Function oxidative
decarboxylation in enzymes PDHC, aKGDHC, and
transketolase Deficiency no aerob glucose
degradation, citric acid cycle, amino acid
degradation leading to ATP-shortage pentosephos
phate pathway can not work, NADPH-deficiency Low
grade deficiency in elderly and restricted, poor
diet loss of appetite, constipation,
depression, peripheral neuropathy, irritability,
fatigue Moderate severe deficiency in chronic
alcoholists Wernike-Korsakoff- syndrome
mental confusion, ataxia (missing
movement coordination), ophtalmoplegia (lower
eye movement capacity) Severe deficiency
beri-beri in alcoholists, in populations who eat
only polished rice muscle atrophy
(disappearance), heart failure
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Demand increased carbohydrate rich food, fever,
trauma, pregnancy, lactation, tea- and coffee
consumers
Source every natural organic food except
polished rice, white flour, refined sugar. It is
found in the cover of the seeds of cereals.
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Vitamin B-2 riboflavin ? FAD, FMN prost.
gr. Producers plants, bacteria Stores yeast,
liver, kidney, egg, milk Function some
dehydrogenases and reductases, all oxidases E.g.
succinate deh., mt. glycerol-3-P deh.,
electrontransport prot. acyl-CoA deh.
dihydrolipoyl deh. glutathione red., NADH deh.,
amino acid oxidases. xanthine oxidase, cytochrome
P450 red., pyruvate deh., ketoglutarate
deh. Deficiency signs in chronic alcoholists
(inflammations) angular cheilitis (lips),
glossitis (tongue), stomatitis (mouth),
photophobia, scaly dermatitis
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Niacin, nicotinic acid, nicotinamide ? vitamin
B3
NAD, NADP
Not really a vitamin, we can synthesize it from
tryptophan, but not enough. Synthesis needsTrp,
pyridoxin, riboflavin, iron. Sourses lean meat,
oily seeds, legumes, liver, fish (in maize Trp
is scarce) Deficiency in starving elderly,
alcoholists pellagra ( rough skin) 4 D
symptoms dermatitis, dementia, depression,
diarrhoea and other mucous membranes
inflammation in GI, and GU tract Function NAD
dehydrogenases characteristic coenzyme NADPH
reductases characteristic coenzyme Demand
increased pregnancy, lactation, chronic illness
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Pantothenic acid vit. B5 ? HS-CoA, ACP
Function acyl-transferases, synthases,
synthetases carboxyl-group joins to it by
thioesther bond. In carbohydrate, lipid,
cholesterol, amino acid metabolism gt 70
enzyme Source every originally living organism,
especially liver, meat, milk, egg, legumes,
mushrooms, fish, fully ground cereals Sensitive
for acids, alkalines and heat Deficiency signs
alone can not occur, just together with other
vitamin B types
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Pyridoxine, pyridoxal, pyridoxamin ? pyridoxal
phosphate vit. B6 PLP
Function Glycogen phosphorylase (here the bigest
amount) Amino acid metabolism1. transaminases
Gly,Ala, Val, Leu, Ile, Tyr, Cys, Glu,
Asp, ornithine 2. amino acid decarboxylases
noradrenalin, dopamin, adrenalin, serotonin,
hisztamin, GABA synthesis 3. hem synthesis (for
hemoglobin, myoglobin, cytochromes) 4.
sfingolipid synthesis (for membranes) 5. Ser,
Thr, Cys, Gly metabolism dehydratases,
aldolases, desulfinases, synthases and lyases,
cleavage enzyme 6. NAD(P) synthesis
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Deficiency signs Irritability, depression,
peripheral neuropathy, seizures, microcytic
anaemia, glucose intolerance, thrombosis,
cardiovascular signs Source meat, vegetables,
fully ground cereals, egg yolk Demand increase
lactation, pregnancy, age, oral
contraceptives consumers, protein rich diet
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Folate folic acid vit. B9 ? THF H4F
tetrahydrofolate
Function Ser, Gly, His, Trp, choline
degradation Met, dTMP, purin ring
synthesis methyl-, methylene, methenyl-,
formimino-, formyl-group transfer Source Every
fresh, not heated, originally living food (cause
heat sensitive) fresh fruits, vegetables Demand
increased lactation, pregnancy
Cause of deficiency intestinal diseases, certain
drugs, improper diet Signs of deficiency
macrocytic anemia, thrombosis, leucocyte number
decreased
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Cobalamin vit. B12
adenosyl-cobalamin, methyl-cobalamin
Function methyl-THF, methyl-Cbl homocystein
methionin
L-methylmalonyl-CoA
succinyl-CoA
Source exclusively bacteria can
synthesize, found in every animal and human
cells not found in plants (strict vegetarians
are in danger) Deficiency signs 1.) blood cells
pruduction decreased, in fast multiplicating
tissues nucleotides, nucleic acids are not
produced megaloblastic anaemia, anaemia
periniciosa 2.) neurologic signs acidosis,
abnormal myelin sheat formation Deficiency can
be because of hereditary transporter defects,
or aquired gut diseases, anacidity, antibodies
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Biotin vitamin B7 biotin Function Coenzyme
of carboxylases gluconeogenesis/citric acid
cycle anaplerotic, lipid synthesis, amino acid
degradation Source nuts, egg, chocolate Every
living organism contains a little, gut
bacteria synthesize Deficiency
signs depression, hallucination, dermatitis,
muscle pain Cause of deficiency exteme
malabsorption, raw egg white regular consumers
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Ascorbic acid vitamin C
Ascorbic acid

• Function
• in collagen Lys and Pro hydroxilation, collagen
  stabilization- adrenal gland adrenalin and
  corticosteroid synthesis
• - nervous system noradrenalin synthesis
• reducing material Fe3 (absorption elevated),
  A- and E-vitamins (antioxidant effect)- folic
  acid absorption increased
• Source fresh plants (It is degraded during
  heating or storage).
• Deficiency signs
• Scurvy pinpoint hemorrhages, bruising,
  osteoporosis (collagen loss) teeth loss, anaemia
  (iron deficient), wound healing impaired, muscle
  weakness

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vitamin K menaquinone, phylloquinone from
animals, from plants Functionin liver
gamma-carboxylation of Gln in blood coagulation
proteins (necessary for membranebinding during
blood coagulation) Deficiency signs
hemophylia Cause of deficiency lipid
malabsorption because of pancreas, bile or
intestinal diseases/ dysfunction qumarin
overdosage, newborn state(not enough in milk)
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Vitamin deficiency often occurs in average
population folate, cobalamin, pyridoxin Vitamin
deficiency can occur in case of improper diet,
alcoholists thiamin, riboflavin, niacin,
ascorbate, phyto/menaquinons Vitamin deficiency
occurs only in extreme starvation or severe gut
diseases panthotenic acid, biotin Heat
sensitives folate, ascorbate, thiamin,
panthotenate Light sensitive riboflavin
(B2-vit) Absorption complicated, problematic,
found only in animals vit. B-12 Some medicines
inhibit their absorption, speed their degradation
or antagonists riboflavin, niacin, pyridoxin,
vitamin K, folate Vitamins alone are not enough,
the proper enzyme action requires minerals and
amino acids (in proper amount and ratio) as well.