Biomedical subjects

Yoshihisa Kato

Publications and source records attributed to Yoshihisa Kato.

3 recordsLinked to original sources

PubMed2003

Depletion of SecDF-YajC causes a decrease in the level of SecG: implication for their functional interaction.

SecA and an apparatus comprising SecYEG and SecDF-YajC complexes catalyze protein translocation across the Escherichia coli membrane. SecDF-YajC and SecG facilitate membrane insertion of SecA, which is the driving force for protein translocation. Here we report that SecDF-YajC depletion together with SecG depletion nearly completely inhibits protein translocation both in vivo and in vitro, although SecDF-YajC had been thought to be unnecessary for in vitro translocation. The level of SecG in membranes decreased to about half upon SecDF-YajC depletion and recovered to a normal level when SecDF-YajC was expressed. SecDF-YajC inhibited disulfide bond formation between two SecG molecules possessing a single cysteine residue. These results suggest functional interaction between SecDF-YajC and SecG.

Antigens, Bacterial↗

PubMed2003

Effects of polychlorinated biphenyls, kanechlor-500, on serum thyroid hormone levels in rats and mice.

Effects of a commercial polychlorinated biphenyls mixture, Kanechlor-500 (KC500), on the levels of serum thyroid hormones such as total thyroxine (T4) and triiodothyronine (T3) were examined comparatively in male Wistar rats and ddy mice. Serum T4 levels were significantly decreased in both rats and mice 4 days after a single ip injection of KC500 (100 mg/kg body weight), whereas decreased levels of T3 were observed in mice but not in rats. In addition, no significant change in the level of serum thyroid stimulating hormone was observed in either rats or mice. Hepatic UDP-glucuronosyltransferases (UDP-GTs) UGT1A1 and UGT1A6, which efficiently mediate glucuronidation of T4 and promote the excretion of the hormones, were induced by KC500 in rats but not in mice. Hepatic microsomal cytochrome P450 (P450) content and the microsomal activity for 7-ethoxy-, 7-pentoxy-, and 7-benzoyloxy-resorufin dealkylations were significantly increased by KC500 in both rats and mice, although the magnitude of increase in the enzyme activities was higher in rats than in mice. The difference in the increase in the activity of microsomal enzymes, including UDP-GT and P450, between KC500-treated rats and mice was not correlated with that in the level of hepatic methylsulfonyl-PCB metabolites. In the present study, we found for the first time that the decrease in serum T4 levels by KC-500 in mice occurred without increase in hepatic UDP-GTs, UGT1A1 and UGT1A6, responsible for T4 glucuronidation. The present findings further suggested that although the decrease in serum T4 levels in KC500-treated rats would occur at least in part through the induction of the UDP-GTs, it might not be dependent on only the increase in the enzymes.

Animals↗

PubMed2003

[Metabolism of 2,3,3',4,4'-pentachlorobiphenyl in hamsters].

The in vivo metabolism of 2,3,3',4,4'-pentachlorobiphenyl (CB105) was studied in hamsters and the effect of cytochrome P450 inducers, phenobarbital (PB) and 3-methylcholanthrene (MC) on its metabolism was compared to rats. After administration of CB105 intraperitoneally at a dose of 3 mg/body, four metabolites, named M-1, M-2, M-3 and M-4, were detected in 5 days-feces of all groups and the formation ratio of the metabolites M-1-M-4 was 1:39:84:0.2 in untreated hamsters and 1:19:6.7:0.7 in untreated rats. On the basis of the mass spectra of four synthetic authentic compounds and the retention times on DB-1 and MPS50 columns, M-1, M-2, M-3 and M-4 were identified as 4'-hydroxy-2,3,3',4,5'-PenCB, 5'-hydroxy-CB105, 5-hydroxy-CB105 and 4-hydroxy-2,3,3',4',5-PenCB, respectively. The pretreatment of PB and MC resulted in about 2-fold fecal excretion of four metabolites in hamsters and in about 3-fold in rats. Of four metabolites, only M-4 were detected in the serum at 5 days after CB105 administration and the concentration was 0.39 microgram/ml of hamster serum and 0.28 microgram/ml of rat serum. In hamsters, the concentration of M-4 was increased to 1.8-fold of untreated animals by PB treatment and 2.6-fold by MC treatment. On the other hand, the treatment of rats with PB and MC did not show such an increase of serum M-4. These results suggested that the hamster oxidized 2,3,4-trichloro-substituted benzene ring predominantly rather than 3',4'-dichloro-substituted benzene ring differently from the rat and that M-4 formed in hamster liver distributed to the blood and retained there to a considerable extent in comparison with that formed in rat liver.

Animals↗