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Biomedical subjects

H Minakami

Publications and source records attributed to H Minakami.

At least 127 records · Page 7Linked to original sources
PubMed1989

Antioxidant activity of probucol. Short communication.

To evaluate a possible antioxidant activity of probucol on NADPH-dependent microsomal lipid peroxidation and on iron-doxorubicin (adriamycin) complex-induced phospholipid peroxidation, the effects were compared with another powerful antioxidant, 2-OH-estrone. Antioxidant activity of 10 mumol/l probucol in NADPH-dependent microsomal lipid peroxidation corresponded to 4 mumol/l 2-OH-estrone. Together with the results obtained from iron-doxorubicin complex-induced phospholipid peroxidation, it was concluded that probucol is a potent inhibitor of lipid peroxidation and has one-quarter to one-half the antioxidant activity of 2-OH-estrone in vitro.

Animals↗
PubMed1988

Mechanism of O2- generation in reduction and oxidation cycle of ubiquinones in a model of mitochondrial electron transport systems.

O2- generation in mitochondrial electron transport systems, especially the NADPH-coenzyme Q10 oxidoreductase system, was examined using a model system, NADPH-coenzyme Q1-NADPH-dependent cytochrome P-450 reductase. One electron reduction of coenzyme Q1 produces coenzyme Q1-. and O2- during enzyme-catalyzed reduction and O2+ coenzyme Q1-. are in equilibrium with O2- + coenzyme Q1 in the presence of enough O2. The coenzyme Q1-. produced can be completely eliminated by superoxide dismutase, identical to bound coenzyme Q10 radical produced in a succinate/fumarate couple-KCN-submitochondrial system in the presence of O2. Superoxide dismutase promotes electron transfer from reduced enzyme to coenzyme Q1 by the rapid dismutation of O2- generated, thereby preventing the reduction of coenzyme Q1 by O2-. The enzymatic reduction of coenzyme Q1 to coenzyme Q1H2 via coenzyme Q1-. is smoothly achieved under anaerobic conditions. The rate of coenzyme Q1H2 autoxidation is extremely slow, i.e., second-order constant for [O2][coenzyme Q1H2] = 1.5 M-1.s-1 at 258 microM O2, pH 7.5 and 25 degrees C.

Anaerobiosis↗
PubMed1988

[Studies on pulsatile secretion of thyrotropin and prolactin in hypogonadal women].

Studies of normal human subjects have shown that prolactin (PRL) as well as thyrotropin (TSH) are secreted in pulsatile fashion. This study was designed to investigate whether or not these two hormones are secreted synchronously. Ten postmenopausal women who had had amenorrhea for at least 3 years and 2 women who had been ovariectomized 3 and 5 years before and were between 35 approximately 60 yr of age were studied. Blood samples were obtained between 1500 approximately 2000 h at 15 min intervals. Distinct pulsatile fluctuation of plasma TSH concentration was present in all subjects. However, only 31% of these pulses were observed to coincide with PRL pulses. The mean (+/- SD) increment of TSH (nadir to peak) was 1.2 +/- 0.5 mu u/ml. The mean interval between pulses of TSH was 73 min. In contrast, regular episodic fluctuation of plasma PRL concentration were present in only 5 out of 12 women, and 48% of these pulses were observed to coincide with TSH pulses. These results indicate that pulses of TSH and PRL are generated independently. Since thyrotropin-releasing hormone (TRH) may be a direct generator of TSH pulse and a potent stimulator of PRL secretion, our results may suggest that physiological concentration of TRH in portal blood which is sufficient to elicit TSH pulse may be too low to elicit PRL pulse.

Adult↗
PubMed1988

[A longitudinal study on the prognosis of ovulatory disturbance in teenage patients with high LH and normal FSH serum levels].

To study the prognosis of adolescent ovulatory disturbance in patients with persistently elevated LH levels (greater than or equal to 25 mIU/ml), normal FSH levels and high LH/FSH (greater than 2.0), 17 patients aged 12-19 years were studied longitudinally for 4-9 years. These 17 patients consisted of 7 patients suffering from amenorrhea with estrogenic effect, 5 patients with functional bleeding, 3 patients with delayed menarche and 2 patients with oligomenorrhea. All of the patients showed exaggerated LH responses to 100 micrograms of LHRH administration while the FSH responses were not different from those obtained from normal women. Out of the 17 patients, 10 (58.8%) patients showed the values of testosterone and 7 (41.2%) androstenedione which were above the mean + 2SD of normal women. Consequently, the mean serum testosterone and androstenedione levels were significantly higher than those in normal women. The mean LH (36.6 +/- 8.3 mIU/ml), FSH (11.2 +/- 1.5 mIU/ml) and LH/FSH (3.3 +/- 0.8) at the age of 21.4 +/- 2.5 years were not different from the mean LH (39.9 +/- 13.3 mIU/ml), FSH (10.8 +/- 1.8 mIU/ml) and LH/FSH (3.8 +/- 1.5) at the age of 16.1 +/- 1.8 years, respectively. None of the 17 patients showed amelioration or deterioration of ovulatory disturbance during long-term observation. To further investigate the central dopamine activity, 10 mg of metoclopramide (MCP) was administered intravenously in these 17 patients. The LH and PRL responses to MCP were evaluated, and the results were compared to those obtained from 17 patients aged over 20 with PCO and from 17 normal women. The LH responses to MCP were positive in this juvenile patient group and the patients aged over 20 PCO group. However, the LH responses to MCP were negative in normal women in both the follicular and luteal phases. In contrast, the PRL responses to MCP were significantly attenuated in juvenile patients and in patients aged over 20 with PCO compared to those in normal women. Since the hormonal profiles in these 17 patients with anovulation or oligo-ovulation were very similar to those in the group aged over 20 with established PCO, it may be suggested that 1) at least part of the adult patients with PCO may have had PCO from late adolescence; 2) the majority of the patients with high LH and normal FSH levels in adolescence will suffer from ovulatory disturbance continuously; 3) in these patients, an aberration of central dopamine in control of LH and PRL may exist.

Adolescent↗
PubMed1988

A new and suitable reconstructed system for NADPH-dependent microsomal lipid peroxidation.

In order to evaluate the O-2 participation in NADPH-dependent microsomal lipid peroxidation, we used reconstructed system which contained detergent-solubilized NADPH-dependent cytochrome P-450 reductase, cytochrome P-450, phospholipid liposomes, NADPH and Fe3+-ADP. Lipid peroxidation, monitored by the formation of thiobarbituric acid-reactive substance, was increased with increasing concentration of detergent-solubilized NADPH cytochrome P-450 reductase, cytochrome P-450 or Fe3+-ADP. Cytochrome P-450-dependent lipid peroxidation was parallel to O-2 generation monitored by chemiluminescence probe with 2-methyl-6-(p-methoxyphenol)-3,7-dihydroimidazo[1,2-a]pyrazin++ +-3-one. Lipid peroxidation was significantly inhibited by superoxide dismutase, but not by catalase or sodium benzoate. The reconstructed system herein described is considered to be very close to NADPH-dependent microsomal lipid peroxidation system.

Animals↗
PubMed1988

Preeclampsia: a microvesicular fat disease of the liver?

To study the interrelationship between preeclampsia, the syndrome of hemolysis, elevated liver enzymes, and low platelet count, and acute fatty liver of pregnancy, 41 liver specimens from 41 preeclamptic women with and without liver dysfunction were examined for the amount of fat deposited in hepatocytes. All 41 specimens stained with oil red O on frozen sections showed a significant amount of microvesicular fat droplets in varying degrees. In contrast, only 11 of the 41 stained conventionally (with hematoxylin-eosin) showed significant fatty infiltration. The density of hepatocellular fat correlated positively with plasma urate concentration and negatively with the platelet count. These findings suggest that preeclampsia may be one of several microvesicular fatty diseases of the liver and that acute fatty liver of pregnancy may be the most severe form.

Adult↗
PubMed1988

Serum luteinizing hormone profile during the menstrual cycle in polycystic ovarian syndrome.

Thirty-three patients with PCO were studied, focusing on the serum LH profile appearing during their menstrual cycles. The elevated LH level declined gradually after ovulation to the normal or near-normal range at the end of the luteal phase and the early follicular phase. The once declined LH level gradually elevated again with the increasing days from the beginning of menstrual flow and remained at a high level until the next ovulation. The LH response to LH-RH increased with the elevating basal LH level. These results may suggest that the timing of hormonal analysis is important for correct diagnosis of PCO.

Adolescent↗
PubMed1988

Prolactin release in polycystic ovarian syndrome.

To evaluate the prevalence of hyperprolactinemia in patients with polycystic ovarian syndrome (PCO), 72 patients with oligo- or anovulation were studied. All of the patients had persisting elevated LH (greater than 25 mIU/ml), normal FSH, high LH/FSH ratio (greater than 2.5), and exaggerated LH responses to LHRH. Mean testosterone and androstenedione concentrations were appreciably increased in these patients. Out of 171 samples for prolactin (PRL) determination from these 72 patients, only 5 patients had a PRL value above 30 ng/ml during the first sampling. The next sampling from these same 5 women disclosed that they were transiently hyperprolactinemic because the next samples showed a normal PRL value. To further investigate the PRL secretory capacity 500 micrograms of TRH and 10 mg of metoclopramide (MCP) were administered to these 72 and 44 patients, respectively. The PRL response to MCP was significantly blunted in these patients compared to normal women while the PRL response to TRH in these patients was not indistinguishable from that in normal women. These results indicate that the true prevalence rate of hyperprolactinemia in PCO may be low rather than high and the association of hyperprolactinemia with PCO may be coincidental rather than a pathogenically related phenomenon.

Adolescent↗
PubMed1988

[Clinical significance of sGOT elevation and thrombocytopenia in preeclampsia patients].

To assess the clinical significance of an elevated liver enzyme (sGOT) on the outcome of preeclamptic pregnancy, the charts of 145 preeclamptic/eclamptic patients who had sGOT determination during 7 days before and 2 days after delivery were reviewed. Of these, 60 patients exhibited a sGOT value above 30U/L (elevated sGOT group). This group was compared with the remaining 85 patients who showed a normal sGOT value related to clinical backgrounds and clinical outcome. The elevated sGOT group had a significantly low platelet count (16.4 +/- 8.4 vs. 21.4 +/- 6.7 X 10(4)/cumm, p less than 0.001) as well as a significantly high perinatal mortality rate (23.8 vs. 6.3%, p less than 0.01). There was a trend to a higher boy-to-girl ratio in the elevated sGOT group than in the normal sGOT group (1.10 vs. 0.83). In a group of 31 patients who were complicated with both elevated sGOT and thrombocytopenia, the perinatal mortality rate increased further to 42.4% and the boy-to-girl ratio was significantly higher than in the group of 66 patients who showed both a normal sGOt and normal platelet count (2.00 vs. 0.85, p less than 0.05). These results may indicate that 1) preeclamptic pregnancies complicated with liver dysfunction may tend to have a low platelet count; 2) liver dysfunction and thrombocytopenia are more likely to become complicated in preeclamptic pregnancies with a male fetus; 3) closer observations would be needed for preeclamptic pregnancy with liver dysfunction and thrombocytopenia.

Adult↗
PubMed1987

Inhibitory effect of progesterone in the postcastration gonadotrophin rise in women.

This study was designed to investigate the effects of progesterone on the gonadotrophin rise after bilateral salpingo-oophorectomy (BSO). Twenty-eight regularly menstruating women underwent hysterectomy and BSO during the follicular phase of the menstrual cycle. They were divided into 5 groups depending on the treatment after BSO. Plasma LH and FSH were studied serially for 14 days after BSO and the patterns of LH and FSH rises were contrasted to those observed in the control group which received neither progesterone nor estrogen. LH and FSH levels in the group which were given low dose progesterone only, rose consistently after BSO and these patterns were similar to those seen in the control group. However, the addition of estrogen reduced gonadotrophin rises significantly more than estrogen did alone. Further, the luteal phase level of progesterone solely has a suppressive effect on the gonadotrophin rises after BSO. Our observations suggest that synergism of progesterone with estrogen may exist in suppressing gonadotrophin secretion in the normal luteal phase and should help in understanding why gonadotrophin levels in the luteal phase are lower than those in the follicular phase of the menstrual cycle.

17 alpha-Hydroxyprogesterone Caproate↗
PubMed1986

Evaluation of GnRH administration on the prolactin response to thyrotrophin-releasing hormone in normal women.

To determine whether GnRH modifies prolactin (PRL) secretion in response to thyrotrophin-releasing hormone (TRH) in normal women, a group of eleven normal women, 23 to 40 years of age, was studied in the mid-follicular phase of the menstrual cycle. The PRL response to TRH was evaluated in serum under control conditions and after GnRH infusion. GnRH administration augmented basal PRL release and amplified TRH-induced PRL release. These results suggest that GnRH may be involved in PRL release, partly by increasing the sensitivity of the lactotrophs to TRH.

Adult↗
PubMed1985

Low serum levels of FSH, LH and prolactin in luteal phase inadequacy.

In order to elucidate the relationship between prolactin (PRL) levels and corpus luteum function in humans, assessment of temporal relationship between levels of PRL, LH, FSH, estradiol and progesterone was made in eleven normal cycling women and six short luteal women. All hormones were determined by specific radioimmunoassay. The mean PRL level in the luteal phase was higher than that in the follicular phase in normal women. On the other hand, no difference mean was seen between the PRL levels of follicular and luteal phases in short luteal women. In addition, follicular and luteal phase secretion of PRL in the short luteal phase (SLP) was lower than that in the normal control. LH and FSH in the follicular and luteal phases, estradiol secretion in the late follicular and early to mid-luteal phases in SLP were also lower than those in the control. These observations were consistent with the hypothesis that SLP is a sequel to aberrant folliculogenesis. In addition, it is inferred that low PRL levels in the SLP might be due to inadequate augmentation by estrogen, rather than giving PRL any positive controlling role in the maintenance of corpus luteum function.

Adult↗
PubMed1985

Effects of progesterone on prolactin secretion in hypogonadal women.

Although estrogen is known to stimulate the secretion of prolactin, there are only slight differences between the prolactin levels in the follicular and luteal phases in normal women. To test the hypothesis that progesterone is involved in the regulation of prolactin release, 50 mg of progesterone was administered intramuscularly at 0600 h to twelve hypogonadal women and blood samples were obtained at 15 min intervals between 1500 and 2000 h to determine the prolactin levels. The day before progesterone treatment, control blood samples were obtained at 15 min intervals between 1500 and 2000 h. The serum progesterone levels were 28.7 +/- 4.1 ng/ml at 1500 h, 24.2 +/- 3.5 ng/ml at 1730 h and 21.3 +/- 2.9 ng/ml (mean +/- SD) at 2000 h. In eight of twelve hypogonadal women, progesterone lowered circulating prolactin levels significantly. These results indicate that a high level of progesterone in the luteal phase may partly block estrogen-induced prolactin release physiologically.

Adult↗