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Results for “Enzyme Induction”

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PubMed1990

Differential enzyme induction of mouse liver and lung following a single low or high dose of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD).

The induction response of cytochrome P-450-dependent enzyme activities to a single low (5 nmol/kg) or high (50 nmol/kg, intraperitoneal [ip] dose of TCDD was examined in liver and lung homogenates over a 12-week time course in an outbred, Ah-responsive strain of mice (National Institutes of Health [NIH] Swiss). Total hepatic cytochrome P-450 was quantified, and the dealkylation of ethoxy- and benzyloxyresorufin (activities of P-450 IA1 and IIB1, respectively) were measured in both tissues at 48 and 96 hr and at 1, 4, and 12 weeks post-TCDD administration. Western immunoblotting with monoclonal antibody 1-7-1 was conducted to confirm the specific IA1-inductive effects of each dose of TCDD over the same time course. Following the low dose, specific IA1 induction was apparent in liver at the earliest time point, was maximal at 1 week, and declined to control values at 12 weeks. Pulmonary IA1 was near-maximally induced at 48 hr, and remained at that level for 4 weeks. In contrast, a tenfold higher dose of TCDD elicited similar IA1 induction profiles for both tissues, with a maximum at 1 week and a progressive loss at 4 and 12 weeks postexposure. P-450 IIB1 activity was elevated in TCDD-treated animals by enzymatic assay; however, Western immunoblotting did not confirm this finding. These data demonstrate persistent dose-dependent P450 induction over many weeks by a single TCDD dose, with significant organ-specific differences: (a) lung is more sensitive than liver to a nonmaximal inducing dose of TCDD, and (b) at a maximally inducing dose of TCDD, lung is very similar to liver in both the level and time course of IA1 induction.

Animals↗
PubMed1977

Angiotensin converting enzyme: induction by steroids in rabbit alveolar macrophages in culture.

Dexamethasone and prednisone in physiologic range increased angiotensin converting enzyme 7- to 16-fold in comparison to control in 3 days at maximal stimulation (4 nM steroid) in rabbit alveolar macrophages in culture. The increase was inhibited by actinomycin D (0.1 microng/ml) and 1 micronM cycloheximide, suggesting that de novo transcription and enzyme synthesis are responsible for the increased enzyme activity. This result is evidence for a regulatory mechanism for angiotensin converting enzyme, which is important in blood pressure control.

Animals↗
PubMed2000

Angiotensin-converting enzyme: induction by hypertension-induced vessel distension.

Vascular angiotensin-converting enzyme (ACE) activity is increased in a variety of disorders representing both early and late stages of atherosclerosis. The factors governing the induction of vascular ACE are poorly understood. We hypothesized that vascular ACE activity might be increased by hypertension-induced vessel distension. Hypertension was induced in rats by suprarenal coarctation of the aorta. Analyses were performed 5 days and 4 weeks post-operation. ACE activity and ACE mRNA level were increased in thoracic aortae from coarctation hypertensive rats that had been exposed to elevated blood pressure, whereas they remained at normal level in abdominal aortae from those rats that had been exposed to normal blood pressure. The degree of aortic ACE induction correlated well with the degree of the trans-stenotic blood pressure gradient. An increase in ACE transcript level was also observed in carotid arteries from coarctation hypertensive rats that had been exposed to elevated blood pressure. In contrast, ACE activity and ACE mRNA expression were not altered in tissues that did not contain any large arteries from coarctation hypertensive rats, although these tissues had been exposed to elevated blood pressure. These results demonstrate an induction of ACE in large arteries that had been exposed to elevated blood pressure, and they imply that the induction of vascular ACE is due to hypertension-induced vessel distension.

Animals↗
PubMed2000

Prostaglandin endoperoxide H synthase mRNA expression in the fetal membranes correlates with fetal fibronectin concentration in the cervico-vaginal fluids at term: evidence of enzyme induction before the onset of labour.

OBJECTIVE: To determine the relationship of prostaglandin endoperoxide H synthase (PGHS) expression in the gestational tissues and fetal fibronectin in cervico-vaginal fluids before the onset of labour at term. DESIGN: Cross-sectional, observational study. SAMPLES: Amnion, chorion laeve and decidua were collected from 24 term pregnant women following elective caesarean section. Samples of cervico-vaginal secretions were obtained from the same women immediately before caesarean section. METHODS: PGHS-1 and PGHS-2 mRNA levels in tissues were determined by specific ribonuclease protection assays. Fetal fibronectin concentrations in the cervico-vaginal fluids were measured by enzyme-linked immunosorbent assay. The abundance of PGHS mRNA was compared between groups of patients with the same mean gestational age but different cervico-vaginal fetal fibronectin levels. Linear regression analysis was used to determine the association between PGHS levels and fetal fibronectin. RESULTS: Two groups of women were identified who had significantly different fetal fibronectin values but the same gestational ages. The group with the higher fetal fibronectin concentrations had significantly higher PGHS- 1 and PGHS-2 mRNA levels in the chorion laeve and higher PGHS-2 mRNA levels in the amnion, than the group with lower fetal fibronectin concentrations. PGHS- 1 and PGHS-2 mRNA levels in the chorion laeve and PGHS-2 mRNA in the amnion showed an overall significant association with fetal fibronectin levels. CONCLUSIONS: High concentrations of fetal fibronectin in cervico-vaginal secretions before the onset of spontaneous labour at term are associated with high levels of PGHS-2 mRNA in the chorion laeve and the amnion and of PGHS- 1 mRNA in the chorion laeve. Increased expression of PGHS in these tissues may therefore be involved in the events leading to term birth.

Amnion↗