Glycolysis (Graece γλυκύς glykys 'dulcis‘ + λύσις lysis 'dissolutio') est iter metabolicum in matrice cytoplasmatica percursum conversionum biochemicarum celerium a materia propulsoria externa glucoso C
6
H
12
O
6
ad acidum pyruvicum CH
3
COCOO
+ H+ intergradum ad nullum oxygenium consumentem formationem materiae propulsoriae internae ad usum mitochondriorum et organellarum cytoplasmatis et membranarum cellularium. Fructus secundus ad usum cellulae reactionum redoxidativarum multarum NADH + H+ est.

Cave: notitiae huius paginae nec praescriptiones nec consilia medica sunt.

Summarium glycolysis
+
Ex una molecula glucosi decem reactionibus biochemicis
et duae moleculae acidi pyruvici et duae ATP et duae NADH nascuntur:
α-D-glucosum + 2NAD+ + 2ADP + 2Pi ⟹ 2(pyruvatum) + 2NADH + 2ATP + 2H+ + 2H2O

Varietates, quarum frequentissima et notissima (itaque in hoc loco descripta) est secundum Gustavum Embden et Otto Fritz Meyerhof (Via Embden-Meyerhof), notae sunt.

Quibusdam in cancrorum versio biochemica ab metabolismo mitochondriali ad glycolysem accidere videtur. Inhibitio enim glycolysis sit una diversis strategiis in cancris tractandis.

Glycolysis momentum glycaemiae maius habet.

Significatio et contextus

recensere

Glycolysis est pars catabolismi saccharidi in organismo plurimorum animalium. Ita magnus huius reactionum decursus est, ut non modo imminuantur moleculas monosaccharidi glucosi, sed recipiantur alia etiam commutantia antea monosaccharida, per exemplum fructosum. Sub intentione metabolica forti glycolyse celeriter energia prope locum indigentiae permitti possit, per exemplum prope vesiculas neurotransmissorum.[1]

Usus proximus acidi pyruvici ex oxygenii praesentia pendet. Oxygenio praesente oxidatio in cyclo acidi citrici atque cursu phosphorylationis oxidativae ad aquam et dioxidum carbonii latior fit, absente invicem fermentatio (fermentatio homolactica) ad lactatum.

Ad summam, glycolysis a saccharidis nullo spatio interposito et celeriter energiam creat. Pro vita cottidiana equidem ad energiam efficiendum machinationes metabolismi supplentes necesse sunt. Oxygenio autem absente saccharomycetes glycolysem augebunt et consumptio glucosi aucta simul Effectus Pasteur nominatur.

Locus glycolysis

recensere

Reactiones biochemicae glycolysis in cellula, ibidem in matrice cytoplasmatica fiunt. Praesentia magnesii satis significationem habere videtur, quod dimidiae ( 1, 3, 7, 9, [[#Reactio biochemica 10: Pyruvati kinasis (PK)|10]] [2]) omnium reactionum hoc elemento egent.

Nonnullis protozois organella praecipua, glycosomata nominata, sunt, in quibus enzymi glycolysis inveniuntur. Exemplum protozoi cum glycosomatibus sunt trypanosomatidae, quae trypanosomiasem excitare possunt.

Summarium graduum

recensere

In glycolysi ab una molecula glucosi effecto, duae acidi pyruvici fiunt:

D-Glucosum Acidum pyruvicum
  + 2 NAD+ + 2 ADP + 2 Pi   2   + 2 NADH + 2 H+ + 2 ATP + 2 H2O

Decem gradus accidunt, quorum primi quinque (reactiones biochemicae 1-5) pars praeparatoria et ultimi quinque gradus (reactiones biochemicae 6-10) pars quaestuosa nominantur.

Pars praeparatoria

Gradus Substratum Enzymum Classis enzymarum Annotationes
1 Glucosum Glc Hexokinasis HK Transferasis Cofactor: Mg2+,
Adenosinum triphosphoricum (ATP)
(energia) consumitur
2 α-D-Glucoso-6-phosphatum G6P Phosphoglucosi isomerasis PGI Isomerasis
3 β-D-Fructoso-6-phosphatum F6P 6-Phosphofructokinasis PFK-1 Transferasis Cofactor: Mg2+,
Adenosinum triphosphoricum (ATP)
(energia) consumitur
4 β-D-Fructoso-1,6-bisphosphatum F1,6BP Aldolasis ALDO Lyasis
5 Dihydroxyacetonophosphatum DHAP Triosophosphati Isomerasis TPI Isomerasis

Pars quaestuosa

Gradus Substratum Enzymum Classis enzymarum Annotationes
6 Glyceraldehydro-3-phosphatum GADP Glyceraldehydrophosphati dehydrogenasis GAPDH Oxidoreductasis Nicotinamidum adeninum dinucleotidum
(NADH, baiulus hydrogenii) formatur. Additio phosphati phosphorolysis vocatur.
7 1,3-Bisphosphoglyceratum 1,3BPG Phosphoglycerati kinasis PGK Phosphoglycerati kinasis Cofactor: Mg2+,
Adenosinum triphosphoricum (ATP)
(energia) formatur
8 3-Phosphoglyceratum 3PG Phosphoglycerati mutasis PGM, PGAM Mutasis
9 2-Phosphoglyceratum 2PG Enolasis ENO Lyasis Cofactor: 2 Mg2+,
una molecula aquae liberatur
10 Phosphoenolpyruvatum PEP Pyruvati kinasis PK Transferasis Cofactor: Mg2+,
Adenosinum triphosphoricum (ATP)
(energia) formatur

Gradus glycolysis

recensere

Reactio biochemica 1: Hexokinasis (HK)

recensere
1. A glucoso ad glucoso-6-phosphatum

Hac in reactione prima phosphatum additur et in decima demum removebitur. Iste grex phosphati glucosum ex cellulam evadere prohibet, hexokinasis similem hauritorii glucosi laborans. Cofactor est Mg2+. Kation hydrogenii deponitur.

Haec reactio consumit energiam. ΔG° = -16,7 kJ/mol.

De biochemico Warburg effectus metabolismi maximi in cancro descriptus hac reactione hexokinasis molita est.

D-Glucosum Hexokinasis α-D-Glucoso-6-phosphatum
 
ATP ADP
 
(Mg2+) H+
 

Reactio biochemica 2: Phosphoglucosi isomerasis (PGI)

recensere
2. A glucoso-6-phosphato ad fructoso-6-phosphatum

Fructosi (cum phosphato) formatio.

α-D-Glucoso-6-phosphatum Phosphoglucosi isomerasis β-D-Fructoso-6-phosphatum
 
 
 

Reactio biochemica 3: Phosphofructokinasis (PFK-1)

recensere
3. A fructoso-6-phosphato ad fructoso-1,6-bisphosphatum

Cum energia phosphofructokinasis imponit alium phosphatum in moleculam - brevi bipartita ... Hic quoque Mg2+ cofactor est. Iterum kation hydrogenii deponitur.

Haec reactio consumit energiam. ΔG° = -14,2 kJ/mol.

β-D-Fructoso-6-phosphatum Phosphofructokinasis β-D-Fructoso-1,6-bisphosphatum
 
ATP ADP
 
(Mg2+) H+
 

Reactio biochemica 4: Aldolasis (ALDO)

recensere
4. A fructoso-1,6-bisphosphato ad glyceraldehydro-3-phosphatum et dihydroxyacetonophosphatum

Separatio ex uno pentoso uno ad duos triosos: aldolasis fructosum moleculis duabus phosphati gravidum in partes duas, quaeque unam moleculam phosphati portans, dividit. Solum dihydroxyacetonophosphatum in reactionem proximam (5) ingreditur. Altera substantia, glyceraldehydro-3-phosphatum, reactioni proximae deest, et statim in reactionem sextam (6) transit.

β-D-Fructoso-1,6-bisphosphatum Aldolasis D-Glyceraldehydro-3-phosphatum Dihydroxyacetonophosphatum
 
 
  +  

Reactio biochemica 5: Triosophosphati isomerasis (TPI)

recensere
5. A dihydroxyacetonophosphato ad glyceraldehydro-3-phosphatum

Unitas: Post isomerasem secundam nihil restat aliud quam Glyceraldehydrum cum phosphato.

Dihydroxyacetonophosphatum Triosophosphati isomerasis D-Glyceraldehydro-3-phosphatum
 
 
 

Reactio biochemica 6: Glyceraldehydrophosphati dehydrogenasis (GAPDH)

recensere
6. A glyceraldehydro-3-phosphato ad 1,3-bisphosphoglyceratum

Oxidatio et phosphorylatio (phosphorolysis).

D-Glyceraldehydro-3-phosphatum GAPDH D-1,3-Bisphosphoglyceratum
 
NAD+ NADH++H+
 
Pi H+
 

Reactio biochemica 7: Phosphoglycerati kinasis (PGK)

recensere
7. A 1,3-bisphosphoglycerato ad 3-phosphoglyceratum

Cofactor: Mg2+

Haec reactio consumit energiam. ΔG° = -18,5 kJ/mol).

D-1,3-Bisphosphoglyceratum Phosphoglycerati kinasis D-3-Phosphoglyceratum
 
ADP ATP
 
H+ (Mg2+)
 

Reactio biochemica 8: Phosphoglycerati mutasis (PGM, PGAM)

recensere
8. A 3-phosphoglycerato ad 2-phosphoglyceratum
D-3-Phosphoglyceratum Phosphoglycerati mutasis D-2-Phosphoglyceratum
 
 
 

Reactio biochemica 9: Enolasis (ENO)

recensere
9. A 2-phosphoglycerato ad phosphoenolpyruvatum

Cofactores: Duo ionta Mg2+, alterum ob causam phosphoglyceratorum conformationis appendicis carboxylici alterum ut socius dehydratationis.

D-2-Phosphoglyceratum Enolasis Phosphoenolpyruvatum
 
H2O
 
(2 Mg2+)
 

Reactio biochemica 10: Pyruvati kinasis (PK)

recensere
10. A phosphoenolpyruvato ad acidum pyruvicum

Cofactor: Mg2+; PK-isoformae L, R, M1, et M2 notae sunt.

Haec reactio consumit energiam. ΔG° = -31,4 kJ/mol.

Phosphoenolpyruvatum Pyruvati kinasis Acidum pyruvicum
 
ADP ATP
 
H+ (Mg2+)
 

Morbi et aegrotationes cum glycolysi coniunctae

recensere

Carcinogenesis et cancer

recensere
  Conferatur pagina principalis: cancer (morbus).

Intra formationem cancri (carcinogenesis) transformatio cellularum sanarum in cancrum observatur incrementum glycolysis[3]. Quoque detrimentum mitochondriorum cum versio metabolica ad glycolysem disputatum est[4]. Inhibitio ergo glycolysis est una diversis strategiis in cancris tractandis[5].

Significatio carcinogensis

recensere

Cum glucosi oxidatio (aerobica) cellularum sanarum principalis fons energiae putetur, cancri cellulae autem glycolysem (anaerobicam) praecipue utuntur[6] - etiam in oxygenii praesentia (effectus Warburgiensis[7]). At mutationes programmarum cycli cellularis in carcinogenesi momentum maximum habere putatur. Isoforma M2 enzymi pyruvati kinasis (PKM2) tetramerus tumorigenesem impellere videtur[8].

Nonnulli cancri cum adenoviris oncolyticis incrementum reactionum anapleroticarum ostendunt[9].

Morbi neurodegenerativi

recensere
  Conferatur pagina principalis: Neurodegeneratio.

Commutationes itineris glycolysis mature in morbis neurodegenerativis appareant[10].

  1. Jang S., Nelson J. C., Bend E. G., Rodríguez-Laureano L., Tueros F. G., Cartagenova L., Underwood K., Jorgensen E. M., Colón-Ramos D. A. (Apr 2016). "Glycolytic Enzymes Localize to Synapses under Energy Stress to Support Synaptic Function". Neuron 90 (2): 278-91 
  2. Magnesio omnia kinasium enolasisque egent
  3. Shi Y., Liu S., Ahmad S., Gao Q. (2018). "Targeting Key Transporters in Tumor Glycolysis as a Novel Anticancer Strategy". Curr Top Med Chem: 10.2174/1568026618666180523105234 
  4. Gonzalez C. D., Alvarez S., Ropolo A., Rosenzvit C., Bagnes M. F., Vaccaro M. I. (2014). "Autophagy, Warburg, and Warburg reverse effects in human cancer". BioMed research international: 2014:926729 
  5. Sheng H., Tang W. (2016). "Glycolysis Inhibitors for Anticancer Therapy: A Review of Recent Patents". Recent Pat Anticancer Drug Discov 11 (3): 297-308 
  6. Zhang X., Zhao H., Li Y., Xia D., Yang L., Ma Y., Li H. (2018). "The role of YAP/TAZ activity in cancer metabolic reprogramming". Mol Cancer 17 (1): 134 
  7. Warburg O (1956). "On respiratory impairment in cancer cells". Science 124 (3215): 269-70 
  8. Wong N., Ojo D., Yan J., Tang D. (2015). "PKM2 contributes to cancer metabolism". Cancer Lett 356 (2 Pt A): 184-91 
  9. Dyer A., Schoeps B., Frost S., Jakeman P., Scott E. M., Freedman J., Jacobus E. J., Seymour L. W. (2019). "Antagonism of Glycolysis and Reductive Carboxylation of Glutamine Potentiates Activity of Oncolytic Adenoviruses in Cancer Cells". Cancer research 79 (2): 331-45 
  10. Bell S. M., Burgess T., Lee J., Blackburn D. J., Allen S. P., Mortiboys H. (Nov 2020). "Peripheral Glycolysis in Neurodegenerative Diseases". International journal of molecular sciences 21 (23): 8924 doi:10.3390/ijms21238924

Nexus interni

Plura legere si cupis

recensere