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Biomedical subjects

M Ema

Publications and source records attributed to M Ema.

At least 109 records · Page 6Linked to original sources
PubMed1979

Production of L-serine by Sarcina albida.

Conditions for the production of microbial L-serine hydroxymethyltransferase and for the conversion of glycine to L-serine were studied. A number of microorganisms were screened for their abilities to form and accululate L-serine from glycine, and Sarcina albida was selected as the best organism. Enzyme activity in this organism as high as 0.12 U/ml could be produced in shaken cultures at 30 degrees C in a medium containing glucose, ammonium sulfate, glycine, yeast extract, and inorganic salts. L-Serine was produced most efficiently by shaking cells at 30 degrees C in a reaction mixture containing 20% glycine, 5 X 10(-3) M formaldehyde, and 3 X 10(-4) M pyridoxal phosphate in yields of 22 mg of broth in 5 days. L-Serine was easily isolated in 84% yields by ion-exchange resin.

Bacteria↗
PubMed1976

Nitrogen source primarily supplied by amino acids and the efficacy for maximal growth of rats.

The effect of osmotic pressure of diets on be food intake of young rats was investigated by comparing the nutritional effect of casein with the corresponding amino acid mixture at 3.2% nitrogen level. Changes in the osmolarity of diets due to the type of dietary carbohydrate had a little effect on food intake, whereas partial substitution of casein for amino acids resulted in significant increase in food intake. Weight gain and food intake of rats fed the 25% replaced amino acid diet were compared with those of rats fed the casein diet. Food intake was lower at 12.5% replacement than at 25% replacement. These observation suggest that a well-balanced amino acid mixture supported maximal growth of rats when 25% of the amino acid mixture was replace with casein. This suggestion could be experimentally confirmed by using an amino acid mixture based on the amino acid composition of whole-egg protein.

Amino Acids↗
PubMedDate not supplied

Comparative developmental toxicity of di-, tri- and tetrabutyltin compounds after administration during late organogenesis in rats.

Dibutyltin dichloride (DBT), tributyltin chloride (TrBT) and tetrabutyltin (TeBT) were compared for their developmental toxicity and teratogenic potential following administration during the susceptible period for teratogenesis of TrBT. Pregnant rats were given either DBT or TrBT at a dose of 165 or 330 mumol kg-1 or TrBT at a dose of 330, 660, 1320, 2640 or 5280 mumol kg-1 on days 13-15 of pregnancy. Treatment with DBT at 165 and 330 mumol kg-1 caused a significant decrease in the maternal body weight gain. A significant decrease in the fetal weight occurred at 165 and 330 mumol kg-1. No significantly increased incidences of postimplantation loss or of fetuses with malformations were found following treatment with DBT. Treatment with TrBT at 165 and 330 mumol kg-1 resulted in a significant decrease in the maternal weight gain. A significant decrease in the fetal weight was found at 330 mumol kg-1. A significantly and markedly increased incidence of fetuses with cleft palate was noted in both groups treated with TrBT. Treatment with TeBT caused a significantly decreased maternal body weight gain at doses of 660 mumol kg-1 and above. A significantly increased incidence of fetuses with cleft palate was observed at a dose of 5280 mumol kg-1. It could be concluded that there is a difference in the manifestation and degree of developmental toxicity between DBT, TrBT and TeBT.

Abnormalities, Drug-Induced↗
PubMedDate not supplied

Developmental effects of di-n-butyl phthalate after a single administration in rats.

The objective of this study was to determine the susceptible day for the developmental toxicity of di-n-butyl phthalate (DBP). Pregnant rats were given a single dose of DBP by gastric intubation at 1500 mg kg(-1) on one of days 6-16 of pregnancy. A significant increase in the incidence of postimplantation loss was found in pregnant rats given DBP on one of days 6-16, except for days 7 and 11. Significant increases in the incidences of fetuses with skeletal malformations, of fetuses with skeletal and internal malformations and of fetuses with external and skeletal malformations were noted after a single dosing of DBP on day 8, on day 9 and on day 15, respectively. Deformity of the cervical vertebrae was frequently observed after administration of DBP on day 8. Deformity of the cervical and thoracic vertebrae and ribs and dilatation of the renal pelvis were predominantly found in fetuses of dams treated with DBP on day 9. Cleft palate and fusion of the sternebrae were exclusively detected after administration of DBP on day 15. It could be concluded that the manifestation of deviant development induced by DBP varies with the developmental stage at the time of administration and that DBP induces two discrete responses from embryos to teratogenicity on days 8 and 9 and on day 15 of pregnancy.

Abnormalities, Drug-Induced↗
PubMedDate not supplied

Developmental effects of plasticizer butyl benzyl phthalate after a single administration in rats.

The objective of this study was to determine the susceptible day for the developmental toxicity of butyl benzyl phthalate (BBP) by a single administration on one of the days during organogenesis. Pregnant rats were given a single dose of BBP by gastric intubation at a dose of 1000 mg kg(-1) on one of days 13-15 of pregnancy and at 1500 mg kg(-1) on one of days 6-16 of pregnancy. Post-implantation embryolethality was found in pregnant rats given on one of days 6-16, except for day 7. Teratogenicity was noted after a single dosing of BBP on one of days 6, 7, 9, 10, 12, 14 and 15. Deformity of the cervical vertebrae frequently was observed after administration of BBP on day 7. Cleft palate and fusion of the sternebrae were found exclusively, after administration of BBP on day 15. It can be concluded that the manifestation of deviant development induced by BBP varies with the developmental stage at the time of administration and that BBP induces two discrete responses from embryos to teratogenicity during early and late organogenesis.

Animals↗
PubMedDate not supplied

Comparative developmental toxicity of butyltin trichloride, dibutyltin dichloride and tributyltin chloride in rats.

Butyltin trichloride (BT), dibutyltin dichloride (DBT) and tributyltin chloride (TBT) were compared for their developmental toxicity including teratogenic potential following administration during the susceptible period for the teratogenesis of DBT. Pregnant rats were given either BT at a dose of 1000, 1500 or 2000 mg kg-1, DBT at a dose of 10 or 15 mg kg-1 or TBT at a dose of 40 or 80 mg kg-1 by gastric intubation on days 7 and 8 of pregnancy. Although maternal toxicity occurred, as evidenced by a significantly increased maternal lethality at 1500 and 2000 mg kg-1 and decreased maternal weight gain at 1000 and 1500 mg kg-1, no significant increase in the incidences of postimplantation loss and malformed fetuses were observed after treatment with BT. Treatment with DBT resulted in a significantly lower maternal weight gain, lower fetal weight and higher postimplantation embryolethality. A significantly and markedly increased incidence of fetuses with malformations, such as exencephaly, cleft jaw, cleft lip, ankyloglossia, club foot, deformity of the vertebral column in the cervical and thoracic regions and of the ribs and ano- or microphthalmia, was observed in both groups treated with DBT. While treatment with TBT at 40 and 80 mg kg-1 caused a significantly decreased maternal weight gain and increased postimplantation embryolethality, no significantly increased incidence of malformed fetuses occurred. It could be concluded that BT, DBT and TBT are different in the susceptibility and spectrum of developmental toxicity.

Abnormalities, Drug-Induced↗
PubMedDate not supplied

Suppression of uterine decidualization as a cause of implantation failure induced by triphenyltin chloride in rats.

In our previous study, triphenyltin chloride (TPTC1) was found to induce implantation failure, as preimplantation embryonic loss, in rats. In this study, the effects of TPTC1 on the uterine function, as a cause of implantation failure, were determined using pseudopregnant rats. Female rats were given TPTC1 by gastric intubation at 3.1, 4.7, and 6.3 mg/kg on pseudopregnant day (PPD) 0 to PPD 3 and the decidual cell response was induced on PPD 4. The uterine weight on PPD 9 served as an index of uterine decidualization. A significant decrease in the uterine weight, which indicates suppression of the uterine decidualization, was detected at 4.7 and 6.3 mg/kg. In our previous study, these doses induced a significant increase in implantation failure in female rats given TPTC1 on gestational day (GD) 0 to 3. The ovarian weight and number of corpora lutea in the TPTC1-treated groups were comparable to that of the controls. A significant decrease in serum progesterone levels after administration of TPTC1 was found at 4.7 and 6.3 mg/kg. These findings suggest that implantation failure due to TPTC1 may be mediated via the suppression of uterine decidualization and correlated with the reduction in serum progesterone levels.

Animals↗
PubMedDate not supplied

Embryolethality of butyl benzyl phthalate during early pregnancy in rats.

In our previous studies, butyl benzyl phthalate (BBP) was found to be embryolethal and teratogenic in rats. In order to extend these findings, the effects of BBP during early pregnancy on maternal parameters were examined. Pregnant rats were given dietary BBP at 2.0% on day 0 through the day of sacrifice, day 7, 9, or 11 of pregnancy. The number of corpora lutea and implantations and the incidence of preimplantation embryonic loss were comparable across all groups. The postimplantation embryonic loss on day 11 in the 2.0% BBP group was markedly higher than that in the control and pair-fed groups. Regardless of the day of sacrifice, the uterine and ovarian weights and plasma progesterone levels, except for the ovarian weight on day 7, in the 2.0% BBP groups were significantly lower than those in the control and pair-fed groups. These findings suggest that the postimplantation embryonic loss due to BBP during early pregnancy is mediated via the reduction in plasma progesterone levels, an impairment of luteal function.

Animals↗
PubMedDate not supplied

Characterization of developmental toxicity of mono-n-benzyl phthalate in rats.

The objective of this study was to characterize the developmental toxicity of mono-n-benzyl phthalate (MBeP), which is one of the major metabolites of n-butyl benzyl phthalate. Pregnant rats were given MBeP by gastric intubation at 250, 375, 500, or 625 mg/kg on days 7 to 9, 10 to 12, or 13 to 15 of pregnancy. A significantly increased incidence of postimplantation loss was found at 500 mg/kg and above regardless of the days of administration. While administration of MBeP on days 7 to 9 or 13 to 15 at 375 mg/kg and above was significantly teratogenic, no evidence of teratogenicity was detected when MBeP was given on days 10 to 12. Deformity of the vertebral column and ribs and dilation of the renal pelvis were frequently observed after administration on days 7 to 9. Cleft palate and fused sternebrae were exclusively found after administration on days 13 to 15. These findings indicate that the susceptibility and spectrum of the developmental toxicity of MBeP vary with the developmental stages at the time of administration.

Animals↗
PubMedDate not supplied

Behavioral effects of acute exposure to tributyltin chloride in rats.

The behavioral effects of a single acute exposure to nonlethal doses of tributyltin chloride (TBTCl) were studied in male Wistar rats. The rats were given TBTCl by oral gavage at doses of 0, 6.3, 12.5, 25.0 or 50.0 mg/kg, and spontaneous motor activity (SMA) and acquisition of conditioned avoidance responses in a shuttle box were monitored. Body weight gain in the 50.0-mg/kg group was significantly lowered, but weight gain in the 6.3-, 12.5- and 25.0-mg/kg groups was comparable to that in the control group. TBTCl caused a dose-related decrease in SMA during the dark phase. The 24-h total daily and 12-h nocturnal activity was decreased at doses of 12.5 mg/kg and above. The acquisition of shock avoidance responses was inhibited in all TBTCl-treated groups in a dose-dependent manner, and the difference was significant for rats given TBTCl at doses of 25.0 mg/kg and above. The data indicate that an acute exposure to TBTCl can cause significant changes in rat behavior and suggest that SMA can serve as a sensitive index for detecting its toxicity.

Analysis of Variance↗
PubMedDate not supplied

Adverse effects of dibutyltin dichloride on initiation and maintenance of rat pregnancy.

The present study was conducted to evaluate the adverse effects of dibutyltin dichloride (DBTCl) on initiation and maintenance of pregnancy after maternal exposure during early pregnancy in rats. After successful mating, female rats were given DBTCl by gastric intubation on Days 0 to 3 or on Days 4 to 7 of pregnancy at 0, 3.8, 7.6, or 15.2 mg/kg. Food-restricted pregnant rats were given an amount of feed equal to the feed intake of female rats treated with DBTCl at 15.2 mg/kg on Days 0 to 3 or on Days 4 to 7 of pregnancy. Female rats were sacrificed on Day 20 of pregnancy and pregnancy outcome was determined. After administration of DBTCl on Days 0 to 3, the rate of nonpregnant females and the incidence of preimplantation embryonic loss in the 7.6 mg/kg group were significantly higher than those in the control group, and those in the 15.2 mg/kg group were significantly higher than those in the control and pair-fed groups. In females with implantations, the numbers of implantations and live fetuses and the incidence of postimplantation embryonic loss in the groups given DBTCl on Days 0 to 3 were not significantly different from those in the control group. The incidence of postimplantation embryonic loss in the groups given DBTCl on Days 4 to 7 at 7.6 and 15.2 mg/kg was significantly higher than that in the control and pair-fed groups. It can be concluded that DBTCl adversely affects initiation and maintenance of pregnancy when administered during early pregnancy and that the manifestations of the adverse effects of DBTCl vary with the gestational stage at the time of maternal exposure.

Animals↗
PubMedDate not supplied

Adverse effects on development of the reproductive system in male offspring of rats given monobutyl phthalate, a metabolite of dibutyl phthalate, during late pregnancy.

The objective of this study was to determine the adverse effects of monobutyl phthalate (MBuP), a major metabolite of dibutyl phthalate (DBP), on development of the reproductive system in offspring following maternal administration during late pregnancy, and to assess the role of MBuP in the antiandrogenic effects of DBP. Pregnant rats were given MBuP by gastric intubation at 250, 500, or 750 mg/kg on days 15 through 17 of pregnancy. Maternal body weight gain and food consumption during the administration period were significantly decreased at 500 mg/kg and higher and at 750 mg/kg, respectively. A significant increase in the incidence of postimplantation embryonic loss was found at 500 mg/kg and higher. The body weights of male and female fetuses were significantly lower at 750 mg/kg. A significant increase in the incidence of fetuses with undescended testes was found at 250 mg/kg and higher. A significant decrease in the anogenital distance (AGD) of male fetuses was observed at 250 mg/kg and higher. The AGD/body weight ratio and AGD/cube root of body weight ratio in male fetuses was also significantly reduced at 250 mg/kg and higher. The AGD, AGD/body weight ratio and AGD/cube root of body weight ratio in female fetuses in the MBuP-treated groups were comparable to those in the control group. The present study indicates that MBuP on days 15 to 17 of pregnancy produced adverse effects on the development of reproductive system in male offspring and suggest that MBuP may be responsible for the induction of the antiandrogenic effects of DBP.

Animals↗
PubMedDate not supplied

Effects of monobutyl phthalate on reproductive function in pregnant and pseudopregnant rats.

The effects of monobutyl phthalate (MBuP) on reproductive function were determined in pregnant and pseudopregnant rats. Rats were given MBuP by gastric intubation at 250, 500, 750, or 1000 mg/kg on days 0 to 8 of pregnancy and pregnancy outcome was determined on day 20 of pregnancy. The effects of MBuP on the uterine function, as a cause of early embryonic loss, were also determined in pseudopregnant rats, with an induced decidual cell response. The same doses of MBuP were given to pseudopregnant rats on days 0 to 8 of pseudopregnancy and the uterine weight on day 9 served as an index of uterine decidualization. MBuP at 1000 mg/kg caused significant increases in the incidences of preimplantation loss in females successfully mated and of postimplantation loss in females having implantations. Uterine decidualization in pseudopregnant rats was significantly decreased at 1000 mg/kg. These findings suggest that early embryonic loss due to MBuP is mediated, at least in part, via suppression of uterine decidualization, an impairment of uterine function.

Administration, Oral↗