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C Marlowe

Publications and source records attributed to C Marlowe.

10 recordsLinked to original sources
PubMed1990

The distribution of [14C]acrylamide in rainbow trout studied by whole-body autoradiography.

The distribution of [2,3-14C]acrylamide was studied in fingerling rainbow trout by whole-body autoradiography. Fish weighing approximately 7 g were injected ip with 3.2 mg/kg [14C]acrylamide (0.1 microCi/g). One group of fish was kept in a fresh flowing water tank and frozen in dry ice/hexane 22 hr after injection; another group was placed in a separate tank of fresh flowing water and frozen 120 hr after treatment. A third group of fish served as nontreated controls. The autoradiographs of the fish at 22 hr show the highest concentration of radioactivity in the kidney, urinary bladder, blood, gallbladder, intestinal contents, and lens of eye. Lesser amounts of radioactivity are seen in the CNS, liver, and gills. Very low concentrations are seen in muscle. By 120 hr the only high concentrations are seen in gallbladder and lens of the eye. Lesser amounts are seen in the sclera, vertebrae, CNS, kidney, wall of intestine, and discrete spots in subcutaneous tissue presumed to be chromatophores. Low amounts are seen in muscle, the tissue usually consumed by man.

Acrylamide↗
PubMed1989

In vivo distribution of a carcinogenic hepatic peroxisome proliferator: whole-body autoradiography of [14C]ciprofibrate in the mouse.

The distribution of radiolabel in male mice was studied by whole-body autoradiography at intervals after oral administration of [14C]ciprofibrate, a carcinogenic hepatic peroxisome proliferator. Radioactivity was rapidly taken up by the liver and to a lesser extent by the brown fat within 9 h after oral dosing of ciprofibrate. The radioactivity levels in blood, interstitial fluid and fat decreased during the first 3 days after dosing, but the liver remained densely labeled. Between 3 and 27 days after dosing, liver exhibited a stippled pattern as a result of heavier labeling apparently around the central veins. The relatively low levels of radiolabel in extra-hepatic tissues observed after oral dosing, together with the prolonged retention in this region of the liver, is consistent with the hepatotropic effects (i.e. hepatic peroxisome proliferation and development of liver tumors) exerted by this compound.

Administration, Oral↗
PubMed1986

Disposition of [14C]dimercaptosuccinic acid in mice.

Dimercaptosuccinic acid labeled with 14C ([14C]DMSA) was administered to mice iv; the mice were frozen by immersion in dry ice/hexane at 6 and 20 min and 1, 3, 9, and 24 hr after injection. The frozen mice were sectioned and processed for whole-body autoradiography for soluble substances. The radioactivity was highly localized in extracellular fluids such as the subcutaneous, intrapleural, intraperitoneal, and periosteal spaces. There was a pronounced accumulation in the periosteal fluid above that in other fluids during the first hour after injection. Most of the radioactivity was eliminated by the kidney and liver. Pretreatment of a mouse with HgCl2 subcutaneously 1 hr before [14C]DMSA produced an increase in radioactivity in the liver and decrease in lung. A high concentration of radioactivity was seen at the subcutaneous site of injection of the HgCl2. The results are interpreted to indicate that most of the DMSA is in the extracellular space but that it can cross cellular membranes to some extent. The pronounced accumulation in periosteal fluid may be an interaction of DMSA with Ca2+ in this space. No tissue had a pronounced retention of the compound, but lung retained more than most other tissues.

Animals↗
PubMed1979

Cortisone mediated decrease in fetal metabolism of glucose.

14C-Glucose was administered to pregnant mice with and without a teratogenic dose of cortisone. Cortisone decreased the transfer of glucose and its metabolites to the fetus and chorioallantoic placenta while increasing the disposition of these substances in maternal liver and muscle. This shift suggests that cortisone exerts its teratogenic action by depriving the fetus of an adequate supply of carbohydrate during its rapid growth and differentiation.

Animals↗
PubMed1978

Inhibition by metyrapone of the accumulation of nicotine-14C in bronchial epithelium of mice.

Further studies have been conducted in an attempt to define the mechanism of the intense accumulation of radioactivity in bronchial epithelium following the administration of nicotine-14C to mice. Male and female pigmented (C57B1/6J) and nonpigmented (A/HeJ) mice were studied by whole-body autoradiography following administration of either nicotine-14C (methyl- or 2'-labeled) or nicotine-1'-N-oxide-14C. When each of these compounds was administered at the same specific activity the radioactivity retained in the bronchial epithelium was much greater for the methyl-labeled nicotine-14C than for the ring-labeled. Following administration of the N-oxide very little radioactivity was retained at this site and this was seen only at a few time intervals. Pretreatment with NaHCO3, NH4Cl, SKF 525A, piperonyl butoxide, progesterone, cysteamine, phenobarbital or metyrapone prior to the administration of [methyl-14C]nicotine was studied. Metyrapone totally prevented the accumulation of radioactivity in the bronchial epithelium and progesterone reduced this accumulation; the other substances used for pretreatment had no effect on the uptake of radioactivity. These results are interpreted to indicate that the accumulation of nicotine in bronchial epithelium is not accounted for by transcellular pH gradients but is due to a high affinity of nicotine for a cytochrome P-450 in this tissue which demethylates the nicotine. The relationship and significance of metabolism of nicotine in this tissue to metabolism at other sites in the body are discussed.

Animals↗
PubMedDate not supplied

Localization of nicotine-14C, cotinine-14C, and nicotine-1'-N-oxide-14C in tissues of the mouse.

The distrubutions of nicotine-14C (2'- or methyl-labeled), cotinine-14C, and nicotine-1'-N-oxide-14C were studied by whole-body autoradiography in mice and in perfused rabbit lung. The compounds were administered either iv, sc, ip, or by inhalation. Blank sections were also incubated with nicotine-14C and cotinine-14C in vitro. The distributions were compared in a black (C57BL/6J), brown (C57L/J), and albino (A/HeJ) strain and in CD-1 germ-free mice. After administration of nicotine-14C in vivo, radioactivity was localized in all strains in bronchi, nasal mucosa, salivary gland, Harder's gland, liver, kidney, stomach, spleen, pancreas, intestine, bone, gallbladder, and adrenal medulla. In the pigmented strains, it was also localized in melanin in the eye, brain, and hair. Radioactivity did not accumulate in the bronchi of late-term fetuses or the 1-day-old newborn but was present in the 2-day-old and older. Cotinine-14C and nicotine-1'-N-oxide-14C, after iv administration, did not localize in bronchi or nasal mucosa at short time intervals after injection. Frozen sections incubated in vitro did not accumulate either nicotine-14C or cotinine-14C in the bronchi; whereas the affinity for melanin was unchanged. Incubation of fresh, nonfrozen mouse lung and perfusion of rabbit lung in vitro with nicotine-14C produced the same localization of radioactivity in bronchi as that seen after in vivo administration. Preheating the frozen sections or lungs in a microwave oven before incubation did not change the localization of radioactivity in the bronchi or other tissues. The localization of radioactivity in bronchi may be due to metabolism, active transport, or binding of nicotine; this mechanism is destroyed by freezing the tissue.

Animals↗
PubMedDate not supplied

Inhibition of the metabolism of urethane in the mouse by dimethyl sulfoxide (DMSO).

Previous studies from this laboratory have shown that alcohols inhibit the localization of nitrosonornicotine and urethane in tissues of the mouse. Subsequent studies demonstrated that this inhibition of the localization of urethane was apparently due to an almost total inhibition of the metabolism of that compound by ethanol. We now report that dimethyl sulfoxide (DMSO) also almost completely inhibits the localization of urethane metabolites in tissues of the mouse and maintains a high concentration of urethane in blood. Since metabolism is essentially the only route of elimination of urethane in the mouse, this indicates that DMSO inhibits the metabolism of urethane. These studies lend further support to the suggestion that urethane is metabolized by either an alcohol dehydrogenase, an aldehyde dehydrogenase, or an alcohol-preferring isozyme of cytochrome P-450. These results indicate that studies on the metabolism as well as the carcinogenic activity of urethane (and possibly other chemicals) also may be affected by concurrent administration of DMSO.

Animals↗