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Biomedical subjects

J C Carlson

Publications and source records attributed to J C Carlson.

At least 55 records · Page 3Linked to original sources
PubMed1981

Compositional and physical properties of microsomal membrane lipids from regressing rat corpora lutea.

Wide angle x-ray diffraction has revealed that during corpus luteum regression there is a liquid-crystalline to gel phase transition in the phospholipid molecules of the cellular membranes. In the present study we have examined the lipid composition of these membranes and looked for evidence of membrane protein involvement in this change. Lipid analysis of smooth microsomal membranes prepared from rat corpora lutea revealed no significant change in the cholesterol to phospholipid ratio or in the ratio of unsaturated to saturated fatty acids with advancing luteolysis. In addition, there was no clear trend for these changes in the relative proportions of the major fatty acids. Liposomes were prepared from smooth microsomal fractions of regressing rat corpora lutea, and examination of these lipid vesicles by x-ray diffraction revealed that the temperature of the liquid-crystalline to gel phase transition was much lower (approximately 25-30 C) than that for the corresponding microsomes. These observations are consistent with the view that membrane proteins contribute to the ordering of lipid that results in a mixture of liquid-crystalline and gel phases in membranes from regressed corpora lutea.

Animals↗
PubMed1981

Assessment of the luteolytic potency of various prostaglandins in the pseudopregnant rabbit.

The ability of systemic infusion of arachidonic acid and various prostaglandin (PG) compounds to induce luteolysis was examined in the Day 9 pseudopregnant rabbit. Administration of PGF-2 alpha (25 microgram/h for 6 h) elicited a decline in plasma progesterone from mean +/- s.e.m. pretreatment levels of 8.83 +/- 0.54 to 0.54 +/- 0.05 ng/ml on the following day (P less than 0.01). A shorter infusion (25 microgram/h for 3 h) or a lower hourly dose rate (12.5 microgram/h for 6 h) of PGF-2 alpha was ineffectual, suggesting that a dose/duration regimen exists for PGF-2 alpha-mediated luteolysis. PGE-2 (25 microgram/h for 6 h) or sodium arachidonate (667 microgram/h for 6 h) did not significantly affect luteal function. Of the PGF-2 alpha metabolites examined, 13,14-dihydro-PGF-2 alpha was the most effective: it was approximately 4-fold more potent as a luteolysin than PGF-2 alpha since functional regression occurred with infusion of 6.25 microgram/h for 6 h. These data illustrate that systemic infusion of PGF-2 alpha is capable of inducing luteolysis in the rabbit. The metabolite 13,14-dihydro-PGF-2 alpha may also be involved luteolytically in this species.

Animals↗
PubMed1979

A new perspective on the mechanism of corpus luteum regression.

Wide angle x-ray diffraction has been used to examine the phase behavior of microsomal membranes from regressing corpora lutea of prepubertal pseudopregnant rats. During periods of optimal progesterone secretion, all of the membrane lipid was in the liquid-crystalline phase at physiological temperature and, therefore, was fluid. However, mixtures of liquid-crystalline and gel phase lipid were observed under identical conditions in microsomal membrane preparations from animals undergoing spontaneous or prostaglandin F2 alpha-induced regression. This was accompanied by a parallel rise in the lipid phase transition temperature. In addition, the proportion of lipid in the gel phase increased with time after prostaglandin F2 alpha treatment. These results indicate that the mechanism of corpus luteum regression may involve phase changes in the phospholipid bilayer of cellular membranes. The resulting presence of gel phase lipid in the membrane matrices could contribute to the loss of tissue function.

Animals↗
PubMed1979

Prostaglandin-stimulated LH release in cyclic and ovariectomized rats.

The ability of prostaglandin (PG) E2 treatment to stimulate luteinizing hormone (LH) release was compared in cyclic (4-day) and ovariectomized rats. PGE2 (500 micrograms) was injected sc and plasma LH concentration was determined in serial jugular blood samples. Administration of PGE2 at 13.30 h on each day of the oestrous cycle resulted in a significantly greater increase in plasma LH levels at pro-oestrus and oestrus than at dioestrus 1 and 2. This differential response by the hypothalamo-hypophyseal axis during the oestrous cycle implicates regulatory activity by ovarian steroid feedback. In oestrogen-primed ovariectomized rats, PGE2 administration stimulated a significant increase in plasma LH, but similar treatment in non-primed castrates decreased plasma LH levels. This finding suggests a major role for oestrogen in regulating this response.

Animals↗
PubMed1979

The effect of LH-RH administration on LH release in the female rabbit.

Intracarotid infusion of LH-RH to female rabbits stimulated a significant increase in plasma LH concentration in the jugular vein. This response varied with the reproductive state of the animal, with a greater release occurring in oestrous (spontaneous or oestrogen-induced) and non-receptive does than in pseudopregnant or ovariectomized animals. If ovariectomized rabbits were pretreated with oestrogen, the pituitary response to LH-RH was restored. These findings suggest that there is little change in pituitary sensitivity to LH-RH infusion between oestrous and non-receptive rabbits, although pseudopregnancy (high physiological levels of progesterone) or ovariectomy inhibit its ability to respond to a releasing-hormone stimulus.

Animals↗
PubMed1978

CL regression in the pseudopregnant rabbit and the effects of treatment with prostaglandin F-2alpha and arachidonic acid.

During pseudopregnancy in the rabbit, plasma progesterone levels in the posterior vena cava fell rapidly from maximal concentrations of 9.8 +/- 0.7 (s.e.m.) ng/ml on Day 13 of pseudopregnancy to 2.0 +/- 0.6 ng/ml on Day 15. There was no significant increase in PGF levels at this time, although administration of indomethacin to a similar group of does delayed functional regression for over 7 days. Subcutaneous injection of 1 mg PGF-2alpha or 35 mg arachidonic acid on Day 9 of pseudopregnancy resulted in loss of luteal function as plasma progesterone levels fell significantly from about 6 to less than 1 ng/ml within 24 h. These findings indicate that the uterine factor responsible for luteolysis in the pseudopregnant rabbit may not be released in the form of PGF-2alpha.

Animals↗
PubMed1977

The effects of prostaglandin and mating on release of LH in the female rabbit.

The release of LH in response to prostaglandin (PG) treatment of female rabbits in various reproductive states was compared with the surge following mating. Intracarotid infusion of PGE-2 or PGF-2alpha (0-3--900 microgram/h) into non-receptive and pseudopregnant does resulted in small, 2--4-fold elevations in jugular vein LH concentration. Similar doses of PGF-2alpha in oestrogen-pretreated, oestrous does stimulated a 13-fold increase in plasma LH levels. Mating resulted in a much larger release of LH, as plasma levels increased approximately 60-fold from 1-1 +/- 0-2 (S.E.M.) ng/ml to 67-8 +/- 10-5 ng/ml. These results indicate that PG can stimulate the hypothalamic-hypophysial axis to release LH in non-receptive, pseudopregnant and oestrogen-pretreated, oestrous rabbits.

Animals↗
PubMed1976

Prostaglandin F2alpha production by the brain and its role in LH secretion.

The arteriovenous difference in the concentration of prostaglandin F2alpha (PGF2alpha) across the brain of the anestrous sheep was measured before and during the induction of luteinizing hormone (LH) secretion with estradiol-17beta (E2-17beta). The results indicate that (a) the brain is a significant source of PGF2alpha, (b) the release of PGF2alpha from the brain occurs in pulses with a circhoral rhythm, and (c) the process through which estrogen exerts its negative and positive feedback effects on LH secretion may depend upon amplitude modulation of PGF2alpha output from the brain.

Animals↗
PubMedDate not supplied

The effects of UV radiation and antioxidants on life span and lipid peroxidation in the rotifer Asplanchna brightwelli.

Lipid peroxidation (LP) rates and life span were determined in control and in ulraviolet (UV) irradiated rotifers of the species Asplanchna brightwelli. UV irradiation administered at 6 h of life significantly increased the rate of LP as the rotifers aged; it also produced a significant shortening of rotifer life span. Pretreatment with 20 microg/ml of vitamin E blocked the increase in LP and the decrease in life span induced by UV radiation. The antioxidant synergist 3,3'-thiodipropionic acid had no such UV-protective effect. These results indicate that the decrease in life span caused by UV radiation may be mediated through the production of lipid peroxides.

Journal Article↗