Biomedical subjects

K Umegaki

Publications and source records attributed to K Umegaki.

At least 37 records · Page 2Linked to original sources

PubMed1998

Influence of one bout of intensive running on lymphocyte micronucleus frequencies in endurance-trained and untrained men.

Exercise induced chromosomal damage was evaluated in trained and untrained subjects, who performed treadmill running at 85% of maximal oxygen uptake for 30 min. The subjects had their peripheral blood taken before, immediately after and 30 min after the running test for the analysis of lymphocyte chromosomal damage that was evaluated by micronucleus assay. The blood samples were also subjected to X-ray irradiation in vitro to examine the modification of exercise induced chromosomal damage by a secondarily induced oxidative stress. Spontaneous chromosomal damage in lymphocytes did not significantly increase at least until 30 min after the running both in the trained and untrained subjects. However, the X-ray-induced chromosomal damage was significantly enhanced at 30 min after the running in the untrained group, but not in the trained group. The ratio of X-ray-induced/spontaneous chromosomal damage also tended to increase after the running only in the untrained group. These preliminary results suggest that intensive exercise induced very slight chromosomal damage only in the untrained group, which could be intensified by the secondarily induced oxidative stress.

Adult↗

PubMed1998

Feeding fish oil to rats accelerates the metabolism of hexachlorobenzene.

This study was conducted to examine the influence of dietary fat on the metabolism and excretion of hexachlorobenzene (HCB), a ubiquitous food contaminant which is metabolized at a low rate. Three groups of rats were fed semi-purified diets containing 10 g/100 g of either soybean oil, lard or fish oil for 2 wk and then given a single dose of HCB by intragastric gavage. The concentrations of HCB and pentachlorophenol (PCP), a major metabolite of HCB, were monitored in the blood for 5 d. Fecal excretion of HCB did not differ among the three groups, indicating no difference in HCB retained in the body among the groups. Concentrations of HCB in blood, liver and brain samples from the lard and fish oil groups, the members of which had a low fat tissue mass, were consistently higher as compared with those in samples from the soybean oil group. The concentration of PCP and the PCP/HCB ratio in the blood were higher in the fish oil group than in the other groups. In addition, the amount of PCP excreted in urine was highest in the fish oil group. The hepatic cytochrome P-450 content in the fish oil group was higher than that in the other groups. These findings indicate that feeding fish oil to rats accelerated HCB metabolism. An increase in hepatic HCB concentration due to a small fat tissue mass and high hepatic cytochrome P-450 content may have played a role in accelerating HCB metabolism in the fish oil group.

Adipose Tissue↗

PubMed1997

Feeding mice palm carotene prevents DNA damage in bone marrow and reduction of peripheral leukocyte counts, and enhances survival following X-ray irradiation.

This study examined the effects of palm carotene feeding on DNA damage of bone marrow, recovery of peripheral leukocyte counts, and the survival of mice that received whole-body X-ray irradiation. The palm carotene was composed of alpha- and beta-carotene in a ratio of 1:3. Mice were fed either a basal diet or a carotene diet (50 mg carotene/100 g diet) for 2 weeks, then irradiated. The carotene diet was prepared by the dietary protocol that markedly enhanced the accumulation of carotene in tissues (J. Nutr. 125, 3081, 1995). DNA damage in bone marrow was evaluated by micronucleus assay using peripheral blood. When mice received X-ray (1.5 Gy), marked DNA damage in bone marrow and reduction of peripheral leukocyte count were observed. These changes were significantly attenuated in mice fed the carotene diet. In addition, X-ray (6.5 Gy)-induced survival of mice fed the carotene diet was higher than those fed the basal diet. In mice fed the carotene diet, alpha- and beta-carotene were detected in bone marrow and liver, and concentration of vitamin A in liver was about four times higher compared with that in mice fed the basal diet. These findings suggest that feeding mice palm carotene prevents radiation-induced damages by way of its antioxidant activity and/or vitamin A activity.

Animals↗

PubMed1997

Hexachlorobenzene accumulated by dams during pregnancy is transferred to suckling rats during early lactation.

The distribution of ingested stable, lipophilic environmental pollutants in dams and their transfer to fetuses and sucklings were investigated in rats fed a diet containing a small amount (35.1 nmol/100 g diet) of hexachlorobenzene (HCB). In the first experiment, we examined the distribution of HCB in pregnant and nursing rats fed the HCB diet during pregnancy and lactation. Its transfer to their sucklings was also studied. On d 16 after parturition, HCB concentrations in the blood, and subcutaneous and perirenal fat of nursing rats fed the HCB diet during pregnancy and lactation were approximately 1/3.5, 1/15 and 1/2.8, respectively, those of pregnant rats fed the HCB diet only during pregnancy. On the other hand, the HCB concentrations in the blood, and subcutaneous and perirenal fat of sucklings were approximately 6, 29 and 15 times higher than those of their dams. Therefore, a large amount of HCB apparently was transferred from dams to suckling pups through the milk. In the second experiment, we fed dams the HCB diet only during pregnancy and determined the distribution of HCB in the pregnant rats and fetuses as well as in the nursing rats and suckling pups. The estimated amount of HCB transferred from a dam to her fetuses corresponded to about 0.39% of her total intake during pregnancy. The amount of HCB detected in nursing rats on d 16 after parturition was much smaller than that in the pregnant rats, suggesting that a large proportion of the HCB that accumulated during pregnancy disappeared from the organs and fat tissues during lactation. The HCB concentration in the stomach contents of suckling pups fed by the dams who had consumed HCB before parturition was highest on d 2 after birth and decreased gradually during the 16 d after birth. In the blood, liver and fat tissues of suckling rats, the HCB concentrations increased until 7 d after birth and then decreased gradually. We conclude that the HCB that accumulated in dams during pregnancy was transferred to their suckling pups through milk in the early days after birth.

Animals↗

PubMed1997

Lack of influence of a long-term high or low vitamin E diet on the oxidative DNA damage in the bone marrow of mice.

To investigate the influence of dietary vitamin E (VE) on DNA damage in bone marrow, we fed mice either a low VE diet (-VE), a basal VE diet (+30 mg VE/kg) or a high VE diet (+1000 mg VE/kg) for 50 weeks. DNA damage was evaluated by two cytogenetic methods: micronucleus (MN) assay using peripheral blood, and examination of sister chromatid exchanges (SCE) in bone marrow cells. The MN assay was performed periodically from 6 to 50 weeks, and showed that the incidence of reticulocytes containing MNs did not increase in the low VE diet group, and did not decrease in the high VE diet group. SCE assay done at 50 weeks also showed no difference among the VE diet groups. VE in bone marrow was markedly lower in the low VE diet group and higher in the high VE diet group compared to that in the basal VE diet group at 6 weeks. The VE at 50 weeks was not markedly different from that at 6 weeks. Corresponding to the changes in the VE, lipid peroxide in bone marrow was higher in the low VE diet group, but was not lower in the high VE diet group. Glutathione and vitamin C in the bone marrow, which were about 100-1000 times higher than that of VE, were not different among the groups.

Aldehydes↗

PubMed1996

Differences in the influence of AIN-purified and non-purified diets on the development of hypertension in SHR and DOCA-salt hypertensive rats.

The influence of non-purified and AIN purified diets on the development of hypertension was examined in deoxycorticosterone acetate (DOCA)-salt hypertensive rats and SHRs. For DOCA-salt hypertensive rats, the development of hypertension was slower in rats fed the AIN 76-purified diet than in those fed the non-purified diet throughout the experimental period of about five weeks. In an experiment using spontaneously hypertensive rats (SHRs), 4-week-old rats were fed either a non-purified diet, a AIN76-purified diet or a AIN93G-purified diet for about nine weeks. In the first 1-2 weeks, the blood pressure was lower in the SHRs fed the AIN93G-purified diet than in those fed the non-purified diet. However, no significant difference in blood pressure was observed within the SHR group thereafter.

Animal Feed↗

PubMed1995

Whole body X-ray irradiation to mice decreases ascorbic acid concentration in bone marrow: comparison between ascorbic acid and vitamin E.

The change in the ascorbic acid concentration in the bone marrow after whole body X-ray irradiation was compared with that in the vitamin E concentration. The ascorbic acid concentration in the bone marrow significantly decreased by 30% 1 h after exposure to 3 Gy of X-rays, whereas the vitamin E concentration in the bone marrow was significantly decreased 5 h after exposure, when the level of ascorbic acid was less than 10% of that in the control. At 24 h after exposure, the ascorbic acid concentration in the bone marrow was significantly decreased by 80% after exposure to 0.5 Gy, whereas the vitamin E concentration was significantly decreased after exposure to 1 Gy or more. In the bone marrow, the decrease in the ascorbic acid concentration was accompanied by a marked increase in the concentration of dehydroascorbic acid, an oxidized form of ascorbic acid. X-ray irradiation did not decrease either the ascorbic acid or vitamin E concentration in the serum or intestine. These findings suggest that the bone marrow is more highly susceptible to oxidative damage by radiation and that ascorbic acid plays an important defense role against it. On Day 8 after irradiation, the decreases in the vitamin E and ascorbic acid concentrations in the bone marrow showed recovery after exposure to 3 Gy, but not after the exposure to 6 Gy.

Animals↗

PubMed1995

Fish oil enhances pentachlorobenzene metabolism and reduces its accumulation in rats.

To investigate the influence of dietary fats on the metabolism and excretion of pentachlorobenzene (PECB), rats were fed semipurified diets containing soybean oil, lard or fish oil (10 g/100 g diet) for 2 wk. Rats then received a single dose of PECB by intragastric gavage. Blood concentration of pentachlorophenol (PCP), a major metabolite of PECB, was higher after 5 h through d 3 and that of PECB was lower after d 5 in the rats fed fish oil than in rats fed the other fats. After d 5, the highest ratio of PCP/PECB in the liver was seen in the fish oil-fed rats. Furthermore, fish oil intake resulted in a markedly lower concentration of PECB in fat tissues, where a large amount of PECB is typically distributed due to its lipophilic property. These findings indicate that fish oil feeding enhances PECB metabolism, thereby decreasing PECB residues in the body. Fish oil-fed rats had a smaller epididymal fat tissue mass compared with lard- or soybean oil-fed rats. The small mass of the fat tissues apparently limited the accumulation of PECB in those tissues and thus accelerated PECB metabolism in the liver.

Adipose Tissue↗

PubMed1995

Simultaneous dietary supplementation of sodium cholate and beta-carotene markedly enhances accumulation of beta-carotene in mice.

This study evaluated whether simultaneous supplementation of sodium cholate and beta-carotene to a diet enhanced the accumulation of beta-carotene in mice. For 2 wk, male ICR mice were fed either a basal diet or a diet containing Dunaliella-bardawil beta-carotene 50 mg/100g that was or was not supplemented with sodium cholate (0.25 g/100 g). The concentrations of beta-carotene in liver and plasma were approximately 5 and 10 times higher, respectively. In the mice fed the beta-carotene diet with sodium cholate than in those fed the beta-carotene diet without sodium cholate. Beta-carotene was not detectable in the liver or plasma of mice fed either basal diet. The concentrations of vitamin E in the plasma and liver of mice fed either beta-carotene diet or the basal diet with sodium cholate were significantly lower than in those fed the basal diet. In a second study, mice were fed a diet containing 50 mg/100 g synthetic beta-carotene supplemented with various concentrations of sodium cholate (0, 0.05, 0.1, 0.25, 0.5 g/100 g) for 2 wk. The concentrations of beta-carotene and vitamin E in plasma, liver and bone marrow cells were higher in mice fed the beta-carotene diet supplemented with 0.05 g/100 g of sodium cholate than in those fed the unsupplemented diet. These findings show that simultaneous supplementation of sodium cholate and beta-carotene to a diet markedly enhances the accumulation of beta-carotene. This dietary protocol may be useful to introduce a high amount of beta-carotene in the tissue of mice in a short period of time.

Animals↗

PubMed1995

Feeding of palm oil carotene to mice did not modify X-ray-induced chromosomal damage in bone marrow cells.

The influence of palm oil carotene treatment on X-ray-induced chromosomal damage in bone marrow cells of mice was studied. Palm oil carotene contains alpha- and beta-carotene in a ratio of 1:3. Mice were fed either a basal diet or carotene diet containing 50 mg of palm oil carotene/100 g for 15 days. On day 13, mice to be X-ray-irradiated received 0.5 Gy of X-ray to their whole bodies, and the chromosomal damage in bone marrow cells was evaluated in terms of the percentages of micronucleated reticulocytes in their peripheral blood on day 15. The chromosomal damage in the X-ray irradiated mice was 10 times higher than that in the unirradiated mice. The feeding of the carotene diet did not prevent the X-ray-induced chromosomal damage. In the bone marrow cells of mice fed the carotene diet, alpha- and beta-carotene were detected, but the concentration of the carotenes was less than one-hundredth of that of vitamin E. In addition, the feeding of carotene diet markedly reduced the concentration of vitamin E in bone marrow cells and serum. The X-ray irradiation reduced the concentration of vitamin C in the bone marrow cells, but did not reduce that of vitamin E or carotene in the cells.

Animals↗

PubMed1994

Decrease in vitamin E levels in the bone marrow of mice receiving whole-body X-ray irradiation.

Mice were subjected to whole-body x-ray irradiation, and changes in vitamin E content and lipid peroxide levels in various tissues were examined. When mice were irradiated with 6 Gy, vitamin E content (per mg protein) in the bone marrow began to decrease 3 h later and a marked decrease to the level of 30% of that of the controls was observed on day 2. Concomitant with the decrease of vitamin E, an increase of lipid peroxide levels was also observed in the bone marrow. On day 2 after an exposure to doses ranging from 1 to 10 Gy, a dose-dependent decrease of vitamin E and an increase of lipid peroxide levels were observed in the bone marrow with a dose of 3 Gy or more. In contrast, neither a decrease of vitamin E nor an increase of lipid peroxide levels was observed in the liver, kidney, spleen, and testes even with an exposure of up to 10 Gy. After the irradiation, glutathione in the bone marrow decreased, while that in the liver increased. These results suggest that the bone marrow is more highly susceptible to oxidative damage induced by radiation than other tissues.

Animals↗

PubMed1994

Effect of beta-carotene on spontaneous and X-ray-induced chromosomal damage in bone marrow cells of mice.

The effect of beta-carotene on spontaneous and X-ray-induced chromosomal damage in bone marrow cells of mice was studied. As a source of beta-carotene, dried Dunaliella bardawil (containing 6% beta-carotene) or oil suspension of Dunaliella beta-carotene was used. In Experiment 1, mice were given a basal diet, a 0.5% Dunaliella diet, or a 4% Dunaliella diet for four weeks. In Experiment 2, mice were given an oil suspension of Dunaliella beta-carotene (300 mg/kg body wt) by gavage for seven days while being fed a fat-rich diet. After beta-carotene treatment for the indicated time, spontaneous and X-ray (0.3 Gy, whole-body)-induced chromosomal damage in bone marrow cells was evaluated in terms of the percentages of micronucleated reticulocytes in their peripheral blood. The beta-carotene treatment slightly lowered the spontaneous and X-ray-induced chromosomal damage in bone marrow cells. Despite the higher doses of beta-carotene, the concentrations of beta-carotene in bone marrow, liver, and serum were much lower than those of vitamin E. In addition, the beta-carotene treatment markedly lowered the concentration of vitamin E in the tissues.

Animals↗

PubMed1994

Beta-carotene prevents x-ray induction of micronuclei in human lymphocytes.

The effects of beta-carotene and ascorbic acid on spontaneous and x-ray-induced appearance of micronuclei (MNs) in human lymphocytes were studied. For 12 d, three groups of healthy volunteers were given beta-carotene-deficient meals containing 100 mg ascorbic acid. There was no supplementation in the first 6 d but, in the last 6 d, the respective groups were given beta-carotene (30 mg), ascorbic acid (300 mg), or placebo. Blood samples were drawn on days 7 and 13 before breakfast, exposed either to x-ray irradiation or left unexposed and were cultured. Lymphocytes containing MNs were then counted. On day 7 the three groups showed comparable MN frequencies. On day 13 lymphocytes containing x-ray-induced MNs became less frequent in the beta-carotene but not the ascorbic acid group. Both before and after the supplementation, the MN frequency of irradiated lymphocytes showed a significant inverse correlation with plasma beta-carotene. These results strongly suggest that beta-carotene protects human lymphocytes from x-ray-induced genetic damage.

Adult↗

PubMed1994

Viscous indigestible polysaccharides reduce accumulation of pentachlorobenzene in rats.

To investigate an effect of indigestible polysaccharides (cellulose as control, sodium alginate, guar gum or lambda-carrageenan) on the accumulation of pentachlorobenzene, male Sprague Dawley rats were fed experimental diets containing 5 g/100 g of these polysaccharides for 2 wk. They were then given orally 80 mumol (20 mg) of pentachlorobenzene along with their respective diets and the residual pentachlorobenzene was determined after 7 d. The ingestion of the viscous indigestible polysaccharides resulted in significantly lower accumulation of pentachlorobenzene in adipose tissue, liver and kidney than that found in rats fed a cellulose diet. Soon (5 h) after pentachlorobenzene administration, its concentration in the blood of rats fed sodium alginate and guar gum was higher than that of rats fed cellulose, but lower in the groups fed all three viscous polysaccharides after d 3. These results indicate that pentachlorobenzene excretion was increased by the ingestion of viscous indigestible polysaccharides. Lower relative weight of adipose tissue, a storage tissue for pentachlorobenzene, was found in the rats fed sodium alginate and guar gum. The lower adipose tissue mass was likely the main contributor to the enhancement of pentachlorobenzene excretion.

Administration, Oral↗

PubMed1994

Improved method for the analysis of ascorbic acid in plasma by high-performance liquid chromatography with electrochemical detection.

We improved the analytical method for the detection of ascorbic acid in plasma by high-performance liquid chromatography (HPLC) with an electrochemical detector (ECD) to be more selective and rapid than the protocol previously used. Main improvements are as follows. Applied potential of ECD to obtain the maximal response for ascorbic acid was +450 mV versus Ag/AgCl, but it was reduced to +350 mV. In that condition, uric acid did not respond to ECD, and only ascorbic acid was detected. EDTA contained in sample extraction/stabilizing solution gave the peak after the ascorbic acid. The addition of EDTA (0.2 mM) to the mobile phase eliminated the EDTA peak. These two improvements gave the chromatogram in which the peak that appeared from the plasma sample was only ascorbic acid, and shorten the sample run time. Ascorbic acid in plasma was unstable even though the plasma was treated with methanol/EDTA: it decreased from 1.5 h at 4 degrees C. However, the treated sample, which was placed at -14 degrees C until the analysis was performed, gave the reliable ascorbic acid value at least up to 6 h. The data obtained from the HPLC-ECD method was consistent with those from the hydrazine method.

Ascorbic Acid↗

PubMed1994

Effect of vitamin E on chromosomal damage in bone marrow cells of mice having received low dose of X-ray irradiation.

When mice had received various doses (0, 0.1, 0.2, 0.4 and 0.8 Gy) of X-ray to their whole bodies, the increased % of reticulocytes with micronucleus (MNs) in peripheral blood, an indicator of chromosomal damage in bone marrow cells, was the highest at 44 hr after the irradiation. At the time, the dose-dependent increase of the % was clearly observed. Using this method, the protective effect of vitamin E on X-ray-induced chromosomal damage was examined. Mice were given various doses (0, 75, 300 mg/kg body weight) of vitamin E by intragastric gavage for 4 days, or fed either a basal vitamin E diet (3 mg % of vitamin E) or a high vitamin E diet (100 mg % of vitamin E) for 5 weeks. Then, the mice were given whole body X-ray irradiation at the dose of 0.3 or 0.4 Gy. Vitamin E concentration in bone marrow cells was significantly elevated by the vitamin E treatment, but was not decreased after irradiation. The vitamin E treatment was unable to inhibit the % of reticulocytes with MNs induced by the irradiation. These results indicate that vitamin E in the bone marrow could not significantly prevent chromosomal damage in bone marrow cells against a low dose of X-ray irradiation.

Animals↗

PubMed1993

Effects of restricted feeding on the absorption, metabolism, and accumulation of pentachlorobenzene in rats.

To investigate the effect of restricted feeding (RF) on the absorption, metabolism, and accumulation of pentachlorobenzene (PECB), rats were fed either ad libitum (AD) or a restricted diet (at 25 or 50% of AD) for 15 days. On the 7th day (day 0), PECB (15 mg/rat) was orally administered. Daily fecal weight and the total amount of PECB excreted into feces were decreased by RF, indicating an increase in PECB absorption due to its prolonged retention in the gastrointestinal tract. However, the amount of PECB excreted was only 4.8% of the dose given to the AD group, and 2.1 and 2.4% of that given to the 50 and 25% restricted diet groups, respectively. The concentrations of PECB and pentachlorophenol, and major metabolite, in blood of the restricted diet groups were higher on day 2 and day 4, while lower on day 6 and day 8 than those of the AD group. On day 8, PECB in liver, kidney, brain, and fat tissue were also lower in the restricted diet groups; the PECB levels in such tissue in the 25 and 50% restricted diet groups were 10-40 and 5-11% of that in the AD group, respectively. These results indicate that PECB metabolism was increased by RF. As PECB is lipophilic, it is most likely that the fat tissue mass, which was markedly decreased by RF, contributed to the enhancement of PECB metabolism. The mechanism seemed to be as follows: as fat tissue mass accumulating PECB decreased, the concentration of PECB in the liver increased, thus the amount of PECB metabolites formed was increased.

Absorption↗

PubMed1993

Influence of dietary vitamin E on the 8-hydroxydeoxyguanosine levels in rat liver DNA.

Rats were fed either a low vitamin E (VE) diet (-VE), a basal VE diet (+VE, 4.5 mg%), or a high VE diet (+VE, 45 mg%) for 7 weeks. VE content, oxidative DNA damage and lipid peroxide levels in their livers were measured. When purified lard was used as a dietary fat, VE content decreased in the low VE group to one-thirtieth of that in the basal VE group; in the high VE group it increased to 4.5-fold that in the basal VE group. Corresponding to the VE levels, lipid peroxide levels increased to 2.7-fold in the low VE group and decreased to two-thirds in the high VE group. The level of 8-hydroxydeoxyguanosine (8-OHdG) in DNA, a marker of oxidative DNA damage, was about 0.6 per 10(5) deoxyguanosine in the basal VE group and comparable values were found in the low VE and the high VE groups. When either soybean oil or safflower oil was used as a dietary fat, VE content and lipid peroxide levels in the liver were also markedly changed in both the low VE group and the high VE group. 8-OHdG levels in DNA of the low VE with safflower oil group tended to be higher than that of the basal and high VE groups. However, no significant difference was observed among them. These results suggest that the change in VE has little influence on the level of oxidative DNA damage in the liver.

8-Hydroxy-2'-Deoxyguanosine↗