Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.2.1.31 (beta-glucuronidase)
 7,680 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The possible sources of biochemical changes in the lung, including changes in activities of lactate dehydrogenase (LDH), beta-glucuronidase (beta-GLU), choline kinase (CHK), and protease inhibitor (PI), as well as protein content, were evaluated following exposure to NO2. Hydroxyurea-induced granulocytopenia attenuated the LDH and beta-GLU responses (46% and 61%, respectively) following acute, but not subacute, exposure to NO2. Increases in PI activity and pulmonary protein content following exposure to NO2 were not altered by inhibition of protein synthesis by cycloheximide. The observed increase in PI activity appears to result from an activation process, whereas a major source of increased pulmonary protein content following exposure appears to occur from leakage into the lung. The response of the lung to irritant insult is thus dynamic, and the contribution from various sources to the biochemical makeup of the lung following irritant insult may depend on the phase of the pulmonary response.
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PMID:Pharmacologic manipulation of the murine pulmonary biochemical response to NO2. 226 87

The biochemical and histopathological response of the lung following acute and repeated (subacute) exposure to nitrogen oxide (NO2) was examined. Activities of lactate dehydrogenase, beta-glucuronidase, choline kinase, and protease inhibitor were measured in murine pulmonary tissue immediately and two days following exposure. Nonenzymatic parameters, pulmonary protein content, and wet lung weight were also monitored. Immediately following acute exposure to NO2, only the nonenzymatic parameters were elevated. By two days following acute exposure, following subacute exposure; however, the nonenzymatic parameters were attenuated with respect to the enzymatic activities. The lung exhibits a dynamic response following damage by oxidants such as NO2. This response is divided into three distinct phases (exudative, proliferative, and tolerant), which can be characterized both biochemically and histopathologically.
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PMID:Phase-dependent response of the lung to NO2 irritant insult. 263 69