Cyanomycin, its identity with pyocyanine.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to J A Last.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Swiss Webster mice were continuously exposed to an atmosphere containing 1.5 ppm ozone (O3) for 5 days. Control mice breathed filtered air. Immediately following the exposure period each mouse was then injected with [1-14C] ascorbic acid. The rate of disappearance of [1-14C] ascorbic acid and the levels of total ascorbic acid were determined in serum, lung, liver, and the remaining carcass over a 9-day period. O3 exposure caused transient decreases in the ascorbic acid levels in liver and serum, whereas lung ascorbic acid levels increased. The apparent biological half-life of ascorbate in carcasses (minus lung and liver) from O3-exposed mice, was significantly prolonged. Significant changes were also observed in the net flux of ascorbic acid in all tissues examined. The results indicated that the change in ascorbic acid levels in a given tissue appeared to reflect changes in the rate of ascorbic acid degradation, its mobilization or tissue compartmentalization, rather than increased synthesis in response to O3 exposure.
We examined the relationship between nicotine-induced vasoconstriction in pregnant rat dams and fetal growth during the third trimester of pregnancy. Pregnant rats were continuously treated between days 13 and 19 of gestation with either nicotine (9.6, 4.8 or 2.4 mg/kg/day), epinephrine (0.72 microgram/kg/day), or saline via continuous infusion from a subcutaneously implanted osmotic minipump. Placental weights in rats treated with high dose nicotine and dams' body weights were severely reduced. However, fetal weights were not affected. Blood flows in uterus and placenta were quantified by measurement of tissue content of 85Sr-labelled microspheres injected via a carotid artery catheter. Both nicotine and epinephrine caused a significant reduction (> 40%) in uterine and placental blood flow. We conclude that vasoconstriction alone as a result of nicotine or epinephrine administration during the last trimester of gestation does not necessarily reduce nutrient supply to the fetus and does not affect fetal growth in rats.