Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: EC:3.5.4.4 (
adenosine deaminase
)
5,136
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
The activity expression and corticosterone inhibition of
adenosine deaminase
(
ADA
) were studied in the spleen, stomach, and liver of mice at various postnatal ages. The specific activity of
ADA
is very low in the spleen and stomach of 5- and 10-day-old mice, and increases significantly (2.5- to 3.0-fold) in 20- and 30-day-old animals. Its level shows a further increase in the spleen of 60-day-old mice while stomach increase of
ADA
is not significant. In contrast, the activity of
ADA
is significantly higher in the liver of 5- and 10-day-old mice, decreases markedly (2.5-fold) in 20- and 30-day-old animals and shows a sharp increase in the liver of 60-day-old mice.
Corticosterone
administration brings a marked inhibition in the activity of
ADA
at all ages studied in the spleen and stomach whereas it inhibits the liver
ADA
only at 30 and 60 days postnatal age. These findings suggest an age- and tissue-specific expression of
ADA
activity and also indicate corticosterone as an inhibitory regulator of this enzyme.
...
PMID:Developmental expression and corticosterone inhibition of adenosine deaminase activity in different tissues of mice. 756 66
Adenosine deaminase (ADA;
EC 3.5.4.4
) is a purine catabolic enzyme causing hydrolytic deamination of adenosine and 2'-deoxyadenosine to inosine and 2'-deoxyinosine. In the present study, the normal endogenous activity level of ADA was investigated in different regions of the gastrointestinal tract (GIT) during postnatal development of chicken. The effects of corticosterone and dibutyryl cAMP (Bt(2)-cAMP) were studied at two selected postnatal ages. The results indicated a significantly high level of ADA at day 1 in all the regions of GIT, which then declined (-34% in esophagus, -35% in crop, and -48% in small intestine) at day 10 and remained fairly constant till day 90. While in the proventiculus, the activity of ADA decreased (-30%) at day 30 and showed further decline (-52%) at day 90 as compared to day 1.
Corticosterone
was seen to significantly decrease (-23 to 79%) the activity level, depending on the regions of GIT studied except proventriculus. The magnitude of decline was more pronounced at day 60 compared to day 10. Bt(2)-cAMP, on the other hand, caused a significant increase (+21 to 67%) in the activity level of ADA again depending on the regions of GIT studied except crop. Western blot analyses also depicted that the decrease and/or increase, respectively, of ADA activity by corticosterone and Bt(2)-cAMP was at the ADA protein level. In conclusion, the study suggests that the ADA activity level is highest at day 1 in all the regions of chicken GIT and could be reduced or enhanced by corticosterone and dibutyryl cAMP, respectively, in an age-specific manner.
...
PMID:Antithetical effects of corticosterone and dibutyryl cAMP on adenosine deaminase in the gastrointestinal tract of chicken during postnatal development. 1922 93
