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TKT  -  transketolase

Bos taurus

 
 
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Disease relevance of TKT

  • Three calves were infected with the parental strain BHV-1 w/t, three with the TK-defective strain, B 1 and four with the HPMPA-resistant strain, 3 A. Inoculation with w/t virus resulted in a reproducible clinical disease characterised by respiratory distress, fever and the presence of virus in nasal mucus [1].
  • The thiamin status (thiamin concentration in whole blood, plasma, and erythrocytes; erythrocyte transketolase activity) of normal cattle consuming varying diets did not differ from that of cattle with polioencephalomalacia or lead poisoning [2].
 

High impact information on TKT

  • The affected animals did not respond to vitamin B1 treatment; the erythrocyte transketolase levels of in-contact cattle and of one untreated affected calf and one untreated lamb were within the normal range [3].
  • Antibody formation after treatment was markedly different in wild type and in TK- virus inoculated groups [4].
  • In the former, virus reactivation was suggested by a sudden rise in serum antibody levels with kinetics closely resembling those reported in infected calves following corticosteroid administration, whereas in the case of the TK- group no significant increase in antibody activity was measured [4].
  • The transketolase activity in beef liver enzyme preparation was extremely inhibited by PRPP and ADP, but the transaldolase activity was not inhibited [5].
  • Transketolase activity in the blood of cattle and sheep in relation to thiamine deficiency [6].
 

Anatomical context of TKT

 

Associations of TKT with chemical compounds

 

Analytical, diagnostic and therapeutic context of TKT

References

  1. The pathogenesis of wild type and drug resistant mutant strains of bovine herpesvirus-1 (BHV-1) in the natural host. Gilliam, S.E., Thackray, A.M., Brown, G.A., Field, H.J. Arch. Virol. (1993) [Pubmed]
  2. Apparent thiamin status of cattle and its relationship to polioencephalomalacia. Loew, F.M., Bettany, J.M., Halifax, C.E. Can. J. Comp. Med. (1975) [Pubmed]
  3. Polioencephalomalacia associated with the ingestion of ammonium sulphate by sheep and cattle. Jeffrey, M., Duff, J.P., Higgins, R.J., Simpson, V.R., Jackman, R., Jones, T.O., Mechie, S.C., Livesey, C.T. Vet. Rec. (1994) [Pubmed]
  4. Experimental reactivation of bovine herpesvirus 1 (BHV-1) by means of corticosteroids in an intranasal rabbit model. Brown, G.A., Field, H.J. Arch. Virol. (1990) [Pubmed]
  5. Inhibitory effect of 5-phosphoribosyl 1-pyrophosphate and ADP on the nonoxidative pentose phosphate pathway activity. Hosomi, S., Tara, H., Terada, T., Mizoguchi, T. Biochem. Med. Metab. Biol. (1989) [Pubmed]
  6. Transketolase activity in the blood of cattle and sheep in relation to thiamine deficiency. Bogin, E., Soback, S., Immelman, A. Zentralblatt für Veterinärmedizin. Reihe A. (1985) [Pubmed]
  7. Diagnostic aspects of cerebrocortical necrosis. Edwin, E.E., Markson, L.M., Shreeve, J., Jackman, R., Carroll, P.J. Vet. Rec. (1979) [Pubmed]
  8. Clinical and biochemical alterations in calves with nutritionally induced polioencephalomalacia. Sager, R.L., Hamar, D.W., Gould, D.H. Am. J. Vet. Res. (1990) [Pubmed]
  9. Biochemical and pathological findings on sheep and calves dying of experimental cerebrocortical necrosis. Horino, R., Itabisashi, T., Hirano, K. J. Vet. Med. Sci. (1994) [Pubmed]
 
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