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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. OxidoreductaseNAD(P) acceptor 1.1.1.1 CH-OH donoralkohol-dehydrogenase. Main enzyme classes: 1. Oxidoreductase2. Transferase - PowerPoint PPT Presentation
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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
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: oxidoreductasesaldehyde group donoroxygen acceptoroxalate oxidase
Main classes:1. oxidoreductases2. transferases3. hydrolases4. lyases5. isomerases6. ligases
1.) Oxidoreductases1.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
2.) Transferases2.1.1. 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. ketogrouptransketolase: 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
2.7. Phosphotransferases = kinases donor: ATPacceptor OH-, COO--, NH2-, HPO4
2-, etc. 2.8.2. Sulfotr. = sulphate transfer
coenzyme: PAPS (phosphoadenosyl-phosphosulfate)
3.) Hydrolases (hydrolysing enzymes)3.1. esterases
carboxyl-, thiol-, phosphate-, sulphate ester hydrolysing3.2. glycosidases: oligo- és polysaccharide cleaving3.4. peptidases, proteases = protein degrading
4.) Lyases addition to double bonds or small molecule elimination4.1. 1.decarboxylases, coenzyme: PLP4.1.3. oxo acid lyases: citrate-synthase or lyase
4.2.1. Hydrolyases: water elimination or addition:fumarase, enolase, akonitase
4.6.1.1. adenylate-cyclase
5.) Isomerases5.1. Racemases and epimerases: one group position changed5.2. cis-trans isomerases5.3.1. aldo-keto isomerases (aldose-ketose)5.3.3. double bond position changers (unsaturated fatty acids)
6.) Ligases = synthetases: ATP, CTP, GTP requiring6.1.1. aminoacyl-tRNA synthetases6.2.1.acyl-CoA synthetases6.3.2. peptid synthetases e.g. glutathione = GSH6.3.5.acid amide producing with Gln donor (GMP, Asn)6.4. carboxylases, coenzyme: biotin
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 arewater soluble
A,D,E,K vitamins are lipid soluble
Coenzyme = loosely bound, easily dissotiated from the enzyme,taking part in catalysis, small organic moleculeNAD, NADP, CoA
Prosthetic group = strictly bound to enzymes, not dissociated, taking part in catalysis, small organic moleculeFAD, FMN, TPP, PLP, THF, DHB, biotin, cobalamine
Effect of alcoholism on the metabolism of vitamins
1.) gastroenteritis, diarrhoea → wrong absorption2.) steatohepatitis, cirrhosis → storing capacity of the liver is decreased
especially pyridoxal, folate, cobalamin3.) competition with acetaldehyde on transport protein → pyridoxin
degradation is increased4.) 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 multiplicatingcells (intestine, skin, blood cells) and big energy requireing organs(nervous system, heart, muscles) can not work properly
Vitamins taking part in amino acid and nucleotid metabolism pyridoxin, folate, cobalamin
In their deficiency the metabolism of amino acids and synthesis ofnucleotides, 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, exceptvit. 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
Vitamin B1 = tiamin → TPP= thiamin-pyrophosphate prosthetic group
Function: oxidative decarboxylation in enzymes: PDHC, αKGDHC,and transketolase
Deficiency: no aerob glucose degradation, citric acid cycle, amino acid degradation leading to ATP-shortagepentosephosphate 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 movementcoordination), ophtalmoplegia (lower eye movement capacity)
Severe deficiency = beri-beri: in alcoholists, in populations who eat onlypolished rice: muscle atrophy (disappearance), heart failure
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 seedsof cereals.
Vitamin B-2 = riboflavin → FAD, FMN prost. gr.
Producers: plants, bacteriaStores: yeast, liver, kidney, egg, milk
Function: some dehydrogenases and reductases, all oxidasesE.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
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 coenzymeNADPH: reductases’ characteristic coenzyme
Demand increased: pregnancy, lactation, chronic illness
Pantothenic acid = vit. B5 → HS-CoA, ACP
Function: acyl-transferases, synthases, synthetasescarboxyl-group joins to it by thioesther bond.In carbohydrate, lipid, cholesterol, amino acid metabolism > 70 enzyme
Source: every originally living organism, especially liver, meat, milk,egg, legumes, mushrooms, fish, fully ground cereals
Sensitive for acids, alkalines and heatDeficiency signs: alone can not occur, just together with other vitamin B types
Pyridoxine, pyridoxal, pyridoxamin → pyridoxal phosphate =vit. B6 PLP
Function:Glycogen phosphorylase (here the bigest amount)
Amino acid metabolism:1. transaminases: Gly,Ala, Val, Leu, Ile, Tyr, Cys, Glu, Asp,
ornithine2. amino acid decarboxylases: noradrenalin, dopamin, adrenalin,
serotonin, hisztamin, GABA synthesis3. hem synthesis (for hemoglobin, myoglobin, cytochromes)4. sfingolipid synthesis (for membranes)5. Ser, Thr, Cys, Gly metabolism dehydratases, aldolases,
desulfinases, synthases and lyases, cleavage enzyme6. NAD(P) synthesis
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 contraceptivesconsumers, protein rich diet
Folate = folic acid = vit. B9 → THF = H4F = tetrahydrofolate
Function:Ser, Gly, His, Trp, choline degradationMet, dTMP, purin ring synthesismethyl-, 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 dietSigns of deficiency: macrocytic anemia, thrombosis, leucocyte
number decreased
Cobalamin = vit. B12 adenosyl-cobalamin, methyl-cobalamin
Function: methyl-THF, methyl-Cblhomocystein methionin
L-methylmalonyl-CoA succinyl-CoASource: exclusively bacteria can synthesize,
found in every animal and human cellsnot found in plants (strict vegetarians are in danger)
Deficiency signs:1.) blood cells pruduction decreased, in fast multiplicating tissues
nucleotides, nucleic acids are not producedmegaloblastic anaemia, anaemia periniciosa
2.) neurologic signs: acidosis, abnormal myelin sheat formationDeficiency can be: because of hereditary transporter defects, or
aquired: gut diseases, anacidity, antibodies
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
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
vitamin K = menaquinone, phylloquinonefrom animals, from plants
Function:in 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/ dysfunctionqumarin overdosage, newborn state(not enough in milk)
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/menaquinonsVitamin deficiency occurs only in extreme starvation or severe gut
diseases: panthotenic acid, biotin
Heat sensitives: folate, ascorbate, thiamin, panthotenateLight sensitive: riboflavin (B2-vit)Absorption complicated, problematic, found only in animals: vit. B-12Some 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.