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Biomedical subjects

T Hobara

Publications and source records attributed to T Hobara.

At least 19 recordsLinked to original sources
PubMed2001

Inhibitory effect of 1,1,1-trichloroethane on calcium channels of neurons.

Peripheral neuropathy may remain for some time after 1,1,1-trichloroethane exposure. A variety of Ca2+ channels gives sensory neurons many kinds of transmitting sensory information. We measured calcium currents in sensory neurons from neonatal rat dorsal root ganglion using whole-cell patch-clamp recordings. Trichloroethane reversibly reduced the low-voltage-activated (LVA) and high-voltage-activated (HVA) calcium. The half-inhibitory concentration (IC50) of the HVA and LVA currents was 5.76 x 10(-3) M and 3.99 x 10(-3) M, respectively. The Hill coefficient of the HVA and LVA currents was 0.61 and 1.04, respectively. In assessing voltage dependence for activation and inactivation of calcium currents, only the HVA calcium current was inactivated at greater negative potentials. This may be one of the mechanisms to reduce HVA current. However, activation and inactivation of the LVA currents were not affected by trichlorothane, so inhibition of the LVA currents may have other mechanisms. Calcium currents are thought to be involved in the control of neuronal excitability and neurotransmitter release. The inhibitory effect of trichloroethane on calcium currents may be involved in trichloroethane-induced sensory discomfort.

Animals↗
PubMed2000

Estimation of the lethal toluene concentration from the accidental death of painting workers.

To determine the potentially lethal level of thinner concentration in the air, we measured the concentration of toluene in the blood and others of three patients who suffered severe acute thinner intoxication between 4 January 1996 and 21 April 1997 in Ube city. The concentration of toluene in blood were 30.2 mg/L in died patient, and 13.7 mg/L and 17.5 mg/L in recovered patients, respectively. By extrapolation from the results of our previous toxicokinetic research on toluene poisoning in anesthetized dogs, the fatal concentration of toluene was estimated to be approximately 1800 to 2000 ppm for 1-hour exposure.

Accidents, Occupational↗
PubMed1997

Histopathological changes induced by zinc hydroxide in rat lungs.

Rat lungs were histologically examined at 1, 7, 14 and 28 days following a single intratracheal instillation of zinc hydroxide (1 mM). After one day of treatment, no confirmatory findings were noted. The zinc hydroxide injections were followed by an increase in proliferating cell nuclear antigen labeling indices in both alveolar macrophages and terminal bronchioles. After 7 days, the zinc hydroxide-treated lungs showed thickening of the interstitium with infiltration by alveolar macrophages, and an increase in the grade of Masson's trichrome staining (collagen fiber) in the alveolar interstitium. Thereafter, these morphological changes disappeared. The vehicle- and zinc sulfate (1 mM)-exposed lungs had no abnormalities at any time point. Formazan deposits in alveolar macrophages, formed as a result of nitro blue tetrazolium reduction, were increased in zinc hydroxide-treated lung slices, suggesting that zinc hydroxide stimulated super oxide anion generation from alveolar macrophages. These results show that zinc hydroxide can induce morphological alterations of rat lungs.

Animals↗
PubMed1995

Role of Kupffer cells in rat liver injury induced by diethyldithiocarbamate.

The hepatotoxicity of diethyldithiocarbamate was examined using an in vitro rat liver slice system. Concentration- and time-dependent losses of intracellular K+ and adenosine triphosphate (ATP) levels were observed in rat liver slices incubated with diethyldithiocarbamate at concentrations between 1 and 10 mM over a 4-h period. Histological study revealed perivenous hepatocyte damage. To examine the involvement of Kupffer cells in diethyldithiocarbamate-induced cytotoxicity, rats were injected intravenously with 10 mg/kg of gadolinium chloride (GdCl3) which diminishes Kupffer cell function. Incubation of liver slice preparations from the GdCl3-treated rats with diethyldithiocarbamate showed marked inhibition of the cytotoxicity induced by diethyldithiocarbamate. Moreover, in vitro addition of manganese-superoxide dismutase, a superoxide anion scavenger, or dimethyl sulfoxide (DMSO), a hydroxyl radical scavenger, also showed potent inhibition. However, dexamethasone, an inhibitor of tumor necrosis factor, and N,N'-diphenyl-p-phenylenediamine (DPPD), an antioxidant, showed partial prevention of cytotoxicity. Formazan deposits formed as a result of nitro blue tetrazolium reduction were found in Kupffer cells at an early stage after diethyldithiocarbamate treatment, while lipid peroxidation occurred after 3 h. Both pretreatment with GdCl3 in vivo and addition of DMSO in vitro prevented the increase in lipid peroxidation within the liver slice preparations induced by diethyldithiocarbamate. These findings suggest that Kupffer cell function may be involved in the pathogenesis of diethyldithiocarbamate hepatotoxicity.

Adenosine Triphosphate↗
PubMed1995

Proliferation of hepatocytes and attenuation from carbon tetrachloride hepatotoxicity by gadolinium chloride in rats.

Intravenous injection of gadolinium chloride (GdCl3) at a dose of 10 mg/kg caused an increase in proliferating cell nuclear antigen labeling index and the grade of pyronin positivity (RNA level) in rat liver. In CCl4-exposed rats, pretreatment with GdCl3 also showed a preventive effect of the liver injury both biochemically and histologically. Moreover, the proliferative action preceded the attenuative effect of the liver injury. Results suggest that GdCl3 induces hepatocyte proliferation, and this action of GdCl3 may modify the development of CCl4-induced liver injury.

Alanine Transaminase↗
PubMed1993

[Effects of typhoon-caused power failure on medical care facilities].

In the evening of September 27, Typhoon 19 passed Yamaguchi prefecture. The wind velocity exceeded anything that the local meteorological observatory has ever recorded so far in this area. When the typhoon was off shore near Yamaguchi prefecture, the gale brought down many electric-light poles around Hofu city with power failure in Hofu city continuing for more than a week. At the same time the total number of emergency patients in Hofu area was the most in the prefecture. Because the power failure continued for many days, there was more indirect damage attributable to this power failure than the damage related directly to the typhoon. The capacity of the emergency electric power generator equipment installed in the Central prefectural hospital in Hofu city is the largest in Yamaguchi prefecture. Even while electric power failed completely in the Hofu city area, treatment of most of the emergency patients at this hospital was possible. There is no hospital that has as large an electric generator as the Central hospital has. Had this typhoon hit in another area, the ensuring confusion which might have occurred at hospitals in that area would have put many patients in danger with the power failure in many hospitals. Power consumption needs in hospitals have increased over that expected on the time the hospital was built. Therefore, the electric power generators installed in hospitals are of the times very small and unable to cope with massive electrical outage.

Disasters↗
PubMed1992

Antiulcer mechanism of action of rebamipide, a novel antiulcer compound, on diethyldithiocarbamate-induced antral gastric ulcers in rats.

The mechanism of the inhibitory action of rebamipide, a new mucosal protective drug, was studied using rats with diethyldithiocarbamate-induced gastric antral ulcers. Rebamipide reduced ulcer formation and inhibited the elevation in lipid peroxide concentration in the gastric mucosa. Rebamipide inhibited both luminol- and lucigenin-dependent chemiluminescence of neutrophils activated by formyl-methionyl-leucyl-phenylalanine. Rebamipide did not alter the reduction of cytochrome c induced by the xanthine-xanthine oxidase system or the NADPH-dependent microsomal lipid peroxidation in the liver. These findings suggest that rebamipide prevents diethyldithiocarbamate-induced gastric ulcer formation by inhibiting neutrophil activation.

Alanine↗
PubMed1991

Effects of various mucosal protective drugs on diethyldithiocarbamate-induced antral ulcer in rats.

This study was designed to determine the effects of exogenous Cu,Zn-superoxide dismutase (SOD) and various mucosal protective agents against antral ulcer induced by diethyldithiocarbamate (DDC), inhibitor of Cu,Zn-SOD. Exogenous Cu,Zn-SOD reduced ulcer formation and prevented a decrease in SOD activity in gastric mucosa. This result indicates that maintenance of mucosal SOD activity is essential to prevent the ulcerogenicity of DDC. Many mucosal protective drugs that increase blood flow, mucus secretion, and endogenous prostaglandin failed to prevent ulcer formation and decrease of mucosal SOD activity. Rebamipide, however, significantly reduced ulcerogenesis and maintained mucosal SOD activity. This suggests that rebamipide has new protective effects on gastric mucosa.

Alanine↗
PubMed1990

Role of active oxygen species in diethyldithiocarbamate-induced gastric ulcer in the rat.

Diethyldithiocarbamate, an inhibitor of Cu,Zn-superoxide dismutase, was recently found to be ulcerogenic in the rat stomach, and active oxygen species were found to be responsible for its ulcerogenicity. To clarify which active oxygen species play a role in ulcerogenesis, the effects of various scavengers and iron-chelators were studied. As superoxide dismutase and catalase reduced the ulcerogenesis induced by diethyldithiocarbamate, the superoxide radical and hydrogen peroxide were considered to play a pathogenic role in this ulcer model.

Animals↗
PubMed1990

Gastric mucosal injury induced by chloral hydrate.

Gastric mucosal injury by chloral hydrate (CH) was investigated in the rat. Rats were injected with CH intraperitoneally or subcutaneously. After the CH injection, gastric ulcers appeared in the glandular stomach at 6 h and the ulcer index peaked in 12 h. The minimum dosage of CH to produce ulcers was 400 mg/kg intraperitoneally and 600 mg/kg subcutaneously.

Animals↗