PubMed Health⌕ Search

Biomedical subjects

K Simizu

Publications and source records attributed to K Simizu.

At least 19 recordsLinked to original sources
PubMed2001

Localization of post-traumatic trochlear nerve palsy associated with hemorrhage at the subarachnoid space by magnetic resonance imaging.

PURPOSE: To report evaluation of traumatic trochlear nerve palsy using head magnetic resonance imaging. DESIGN: Observational case reports. METHODS: We examined two cases involving trochlear nerve palsy after closed head injury. RESULTS: Using a fluid attenuated inversion recovery pulse sequence, MRI showed a high-intensity lesion consistent with subarachnoid hemorrhage at the trochlear nerve area in the ambient cisterns. CONCLUSION: An impact force directed toward the tentorium can be a mechanism of injury in some post-traumatic trochlear nerve palsies. Fluid attenuated inversion recovery pulse sequence is a sensitive method for detection of abnormalities in cases associated with head injury.

Adolescent↗
PubMed1995

Prooxidant and antioxidant hepatic factors in rats chronically fed an ethanol regimen and treated with an acute dose of lindane.

While acute lindane treatment and chronic ethanol feeding to rats have been associated with hepatic oxidative stress, the possible roles of these stresses in the pathogenesis of hepatic lesions reported in acute lindane intoxication and in those observed in some models of chronic alcoholism have not been established. Our previous studies in rats chronically fed ethanol regimens and then treated with a single intraperitoneal (i.p.) dose of lindane (20 mg/kg) showed that while lindane per se was invariably associated with hepatic oxidative stress, chronic ethanol feeding only produced this stress when the dietary level of vitamin E was relatively low. Chronic ethanol pretreatment did not significantly affect the lindane-associated oxidative stress, and neither chronic ethanol feeding nor acute lindane, single or in combination, produced any histologic and biochemical evidence of liver damage. In the present experiment, the acute dose of lindane was increased to 40 mg/kg, and we have studied a larger number of prooxidant and antioxidant hepatic factors. Male Wistar rats (115.5 +/- 5.4 g) were fed ad lib for 11 weeks a calorically well-balanced and nutritionally adequate basal diet, or the same basal diet plus a 32% ethanol/25% sucrose solution, also ad lib, and were then injected i.p. with a single dose of lindane or with equivalent amounts of corn oil. The results indicated that acute lindane treatment to naive rats increased practically all the prooxidant hepatic factors examined (cytochromes P450 and b5, NADPH cytochrome c reductase, NADPH oxidase), as well as the generation of microsomal superoxide radical and thiobarbituric acid reactive substances of liver homogenates, but did not modify any of the antioxidant hepatic factors studied. Conversely, the chronic administration of ethanol alone did not significantly affect the prooxidant hepatic factors but reduced some of the antioxidants (i.e., the activities of GSH-Px and the contents of alpha-tocopherol and ubiquinols 9 and 10). Although chronic ethanol pretreatment further increased the superoxide generation induced by lindane per se, it did not increase but generally reduced the effects of lindane per se on the other prooxidant factors studied. Furthermore, although acute lindane administration to ethanol-pretreated rats was associated with decreases in GSH and catalase (not affected by ethanol or lindane treatment alone), it did not substantially modify the reducing effects of ethanol feeding per se on GSH-Px, alpha-tocopherol, and ubiquinols. Once again, neither chronic ethanol feeding nor lindane treatment, single or in combination, was associated with any evidence of liver damage.

Animals↗
PubMed1995

[Diagnosis of Churg-Strauss syndorme with trans-bronchial lung biopsy].

A 69-year-old woman was hospitalized several times because of asthma attacks. Laboratory data revealed an increase in eosinophils and elevation of serum IgE. Both chest radiographs and computed tomography showed fine nodular shadows in both lung fields. Tissue samples obtained by trans-bronchial lung biopsy (TBLB) revealed extra-vascular granuloma. The patient complained of numbness of the extremities and neuron conduction velocity was low. Based on these findings, Churg-Strauss syndrome was diagnosed. Prednisolone improved the patient's symptoms. Patients with this syndrome reportedly respond well if it is diagnosed and treated with corticosteroids early. Chest roentgenography reveals various abnormal shadows in patients with this syndrome. For early diagnosis, TBLB is helpful and comparatively safe. This case was unusual because extra-vascular granuloma was found by TBLB.

Aged↗
PubMed1994

Acute lindane intoxication: a study on lindane tissue concentration and oxidative stress-related parameters in liver and erythrocytes.

Treatment of rats with daily doses of 20 mg of lindane/kg for 3 consecutive days led to the accumulation of the insecticide in several tissues, including erythrocytes and liver. Lindane did not alter the hematocrit and hemoglobin concentration but reduced methemoglobin levels by 17%. Red blood cells from controls and lindane-treated rats, exposed to t-butyl hydroperoxide, exhibited comparable rates of oxygen uptake and visible chemiluminescence, whereas the induction period that precedes oxygen uptake was significantly enhanced in the latter group. Lindane treatment did not modify the activity of erythrocyte glutathione peroxidase, glucose-6-phosphate dehydrogenase, catalase, and methemoglobin reductase, being the total content of glutathione and superoxide dismutase activity significantly increased. The liver from lindane-treated rats showed an enhanced microsomal pro-oxidant activity, evidenced by higher cytochrome P450 content and NADPH-cytochrome c reductase and NADPH oxidase activities. The higher enzyme activities led to an increased superoxide anion generation (adrenochrome formation) and lipid peroxidation (measured either by the production of thiobarbituric acid reactants and spontaneous visible chemiluminescence). Concomitantly, liver glutathione content and the activity of glutathione peroxidase-glutathione reductase couple were augmented by lindane treatment, without any change in superoxide dismutase activity, together with a reduction in that of catalase. Results suggest that lindane does not alter the prooxidant/antioxidant status of the erythrocyte in conditions of a significant cellular accumulation of the insecticide, which might exert direct action on enzymatic systems leading to enhanced superoxide dismutase activity and glutathione content.(ABSTRACT TRUNCATED AT 250 WORDS)

Adipose Tissue↗
PubMed1994

Brain and liver lipid peroxidation levels following acute and short-term lindane administration in the rat.

Oxidative stress-related parameters in rat brain and liver were evaluated following acute (60 mg/kg i.p., 2 and 24 h after dosing) or short-term (1000 ppm in the diet for 90 days) lindane administration. Both treatments elicited a significant accumulation of lindane in brain and liver, with convulsions observed in short-term and 24-h lindane-treated rats. In these conditions, lindane exposure did not alter brain lipid peroxidation, assessed as thiobarbituric acid reactants formation and spontaneous chemiluminescence, parameters that were enhanced in the liver. The activities of antioxidant enzymes in the brain (superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase and glucose 6-phosphate dehydrogenase) were not modified by acute lindane treatment, while brain glutathione content was significantly reduced by 13%. It is concluded that lindane does not alter the oxidative stress status of the brain as occurs in liver, regardless of the time of exposure of rats to either acute or short-term administration of the insecticide.

Animals↗
PubMed1994

Dose-dependent study of liver lipid peroxidation related parameters in rats treated with pp'-DDT.

Rats treated with increasing doses of pp'-DDT (60, 100 and 180 mg/kg body wt.) i.p., for 24 h, showed a dose-independent increase in liver cytochrome P450 levels, together with an increase in lipid peroxidation, measured as production of thiobarbituric acid reactants. This oxidant condition elicited in the liver by DDT was not accompanied by any change in the activity of NADPH-cytochrome c reductase or in the rate of superoxide anion generation by liver microsomal fraction. The activities of superoxide dismutase and glutathione peroxidase were found to be increased in the higher dose DDT-treated rats, without any change in those from catalase and glutathione reductase. The results presented showed an oxidant condition in the liver elicited by DDT treatment of rats, without any adequate hypothesis proposed to explain these data.

Adrenochrome↗
PubMed1993

Differential effects of short-term lindane administration on parameters related to oxidative stress in rat liver and erythrocytes.

Parameters related to oxidative stress in rat liver and erythrocytes were studied after short-term administration (60 and 90 days) of 1000 ppm of lindane in the diet. Lindane induced an oxidative stress condition in the liver, which is related to an enhancement in microsomal NADPH-cytochrome c reductase and NADPH oxidase activities, superoxide radical formation and cytochrome P450 content, produced independently of the time of treatment. Also, decreased activities of glutathione peroxidase and catalase were concomitantly observed. Although these changes were paralleled by an increase in lipid peroxidation indices, such as production of thiobarbituric acid reactants and spontaneous chemiluminescence, no evidence of liver injury was obtained. Lindane treatment did not exert quantitatively important changes in the pro-oxidant/anti-oxidant status of the erythrocyte, with reduction in the red blood cell mass possibly reflecting actions of the insecticide on the erythropoietic process.

Animals↗
PubMed1993

Turnover of hepatic glutathione after acute lindane intoxication.

The administration of lindane (60 mg/kg) to fed rats diminished the content of hepatic glutathione (GSH) 4 h after treatment, which was recovered at 24 h. At these experimental times, the activities of glutathione peroxidase, glutathione reductase, glutathione-S-transferases and gamma-glutamyltransferase in the liver of lindane-treated rats and control animals were comparable. Liver GSH turnover, measured after a pulse of [35S]cysteine, was enhanced by 69% (P < 0.05) in lindane-treated rats 24 h after intoxication compared to controls, with a 63% (P < 0.05) increase in the estimated rate of GSH synthesis. It is concluded that lindane enhances GSH synthesis in rat liver 24 h after treatment as a consequence of the decrement in its content observed at early times of intoxication (4 h), thus allowing the recovery of the normal level of hepatic GSH.

Animals↗
PubMed1991

Liver lipid peroxidation-related parameters after short-term administration of hexachlorocyclohexane isomers to rats.

Rats treated with diets containing 20 ppm of alpha- or gamma-hexachlorocyclohexane (HCH) for 15 or 30 days showed increased levels of liver cytochrome P-450 followed by increased production of both thiobarbituric acid reactants by liver homogenates and microsomes and superoxide anion production by liver microsomes. In these animals superoxide dismutase (SOD) activity was also increased. In consequence, the ratio between SOD activity and microsomal superoxide radical (O2-.) production showed a slight increase after 15 days of treatment. However, after 30 days, there was a tendency for this ratio to decrease. Other parameters studied were liver glucose-6-phosphate dehydrogenase, glutathione peroxidase, glutathione reductase and catalase (CAT) activities. Among them, only CAT activity showed a 26% and 38% increase after 15 or 30 days of treatment with the alpha-isomer. It is suggested that when lipid peroxidation is involved in the mechanism of toxicity of a xenobiotic, this parameter can be used to determine the no-observed-effect level.

Animals↗
PubMed1991

Effects of hyperthyroidism on rat liver glutathione metabolism: related enzymes' activities, efflux, and turnover.

The effect of hyperthyroidism on liver glutathione (GSH) metabolism was studied in fed rats after the administration of 0.1 mg T3/kg body wt, for 1-3 consecutive days. T3-calorigenesis resulted in elevated rates of O2 consumption by the liver, together with higher lipid peroxidative processes and GSH depletion, compared to the euthyroid state. The study of the enzymes related to GSH metabolism revealed no significant changes in the activity of glutathione peroxidase and glutathione reductase, with decreases (27-41%) in the activity of glutathione-S-transferases and marked elevation (133%) in that of gamma-glutamyl transferase, 3 days after T3 treatment. At this experimental time, the activity of the NADPH generating enzyme glucose-6-phosphate dehydrogenase was enhanced by 84% in the liver of T3-treated rats, compared to that in the controls. In these conditions, the canalicular efflux of GSH was not altered by T3, whereas net and fractional rates of sinusoidal GSH efflux were enhanced by 86% and 288%, respectively. The latter effect of hyperthyroidism was found in parallel with an enhancement in sinusoidal lactate dehydrogenase and protein release, suggesting that loss of GSH might be related to a permeabilization of the hepatocyte plasma membrane. Liver GSH turnover assessed after a pulse of [35S]cysteine resulted in a 209% increase in the fractional turnover rate in hyperthyroid rats over controls, under steady state conditions for both hepatic GSH pools, leading to a 62% enhancement in the respective turnover flux. Data suggest that the elevation in the sinusoidal GSH efflux from the liver and in the hepatic capacity to degrade the tripeptide are major mechanisms leading to GSH depletion in the liver of T3-treated rats. As the increased GSH use is not balanced by the elevation in GSH synthesis, a lower steady state level of GSH is attained in the liver.

Animals↗
PubMed1991

Mechanisms of lindane-induced hepatotoxicity: alterations of respiratory activity and sinusoidal glutathione efflux in the isolated perfused rat liver.

1. Lindane (25-60 mg/kg) at 24 h after dosage induced a dose-dependent increase in oxygen consumption by perfused rat livers, an effect not observed at early times (2-6 h) after administration. About 60% of the increase in liver oxygen uptake is suppressed by the antioxidant, desferrioxamine, indicating enhanced free radical activity induced by the insecticide. 2. The hepatic content of total GSH equivalents (GSH + 2GSSG) decreased 4 h after lindane treatment (60 mg/kg), together with significant diminution in net and fractional rates of sinusoidal GSH efflux, that returned to control values 24 h after treatment. 3. These data indicate that lindane resulted in marked changes in hepatic oxidative capacity and glutathione metabolism, which condition the production of oxidative stress in the liver at different times of intoxication.

Animals↗
PubMed1991

Effect of phenobarbital and 3-methylcholanthrene on the early oxidative stress component induced by lindane in rat liver.

1. Lindane administered to untreated rats or rats pretreated with phenobarbital (PB) or 3-methylcholanthrene (MC) increased liver lipid peroxidation, of the same magnitude in all groups. 2. PB pretreatment produced a 50% increase in lipid peroxidation (TBAR) by liver homogenates and microsomes, an effect accompanied by increases in cytochrome P-450, NADPH-cytochrome P-450 reductase, NADPH oxidase and microsomal superoxide anion production, MC pretreatment resulted in increases in liver cytochrome P-450 and NADPH oxidase only. 3. Pretreatment of rats with PB, but not MC or lindane, gave increases in glutathione peroxidase and reductase. 4. Pretreatment with PB, but not MC, increased liver GSH. Lindane decreased liver GSH to the same extent as PB plus lindane. 5. Biliary GSH, GSSG and bile flow were decreased by lindane to similar extents in all groups. 6. Lindane induced periportal necrosis with haemorrhagic foci in all groups. 7. Data presented indicate that the early lipid peroxidative response of liver to lindane was unchanged by PB- or MC-stimulated hepatic microsomal enzyme induction.

Animals↗
PubMed1991

Ability of young children to button and unbutton clothes.

From 2 years of age, children enjoy trying to button and unbutton their jacket. The clothing of the children at this stage should have the form which fits their motor skills so as to develop their interest in buttons and to help their study in manipulating buttons. We observed processes of dressing and actions of buttoning and unbuttoning at the nursery school, for children in the 3.3-5.9 year range. Also, we experimented about dressing mainly for children in 2 year range to observe the process of manipulating buttons. As factors of experiment, we took two buttonhole directions (vertical and across) and three sizes of buttons (1, 2, 3 cm). The direction of buttonholes was significant at the 5% level. We recognized that buttonholes in the vertical direction were easier for children to button. We came to the following conclusion: for an open front of children's clothing, buttons having a 2 cm diameter and buttonholes in the vertical direction were the best.

Age Factors↗
PubMed1990

[Investigation of etiologies for acute renal failure due to rhabdomyolysis in 5 patients].

We experienced 5 cases of acute renal failure due to rhabdomyolysis during the last two years and investigated those etiologies. Diagnosis of rhabdomyolysis was established by the detection of elevated serum creatine phosphokinase, myoglobin, aldolase, myoglobinuria as well as by the clinical course. The respective underlying illness of the 5 cases were grand mal seizures, infection (high fever), heat stroke, diabetes mellitus with hyperosmolar nonketotic coma and cerebral infarction treated by barbiturate. In this investigation, however, any single cause was not enough as the etiologies of rhabdomyolysis. There were multiple factors responsible to rhabdomyolysis in each case, such as hypokalemia, hypophosphatemia, shock, arteriosclerosis, etc. Some cases could not be classified as traumatic or non-traumatic rhabdomyolysis. Thus, in one case, acute renal failure due to rhabdomyolysis induced by the combination of grand mal seizures and serum potassium/phosphate depletion. 2 cases recovered without hemodialysis. 3 cases died in multiple organ failure, included a case treated by hemodialysis. We conclude that acute renal failure due to rhabdomyolysis induced easily by numerous diseases and early diagnosis is recommended.

Acute Kidney Injury↗
PubMed1989

Lindane-induced liver oxidative stress: respiratory alterations and the effect of desferrioxamine in the isolated perfused rat liver.

The effects of lindane administration (25-60 mg kg-1 for 24 h) on hepatic oxygen consumption were studied in the isolated perfused rat liver, in the absence and presence of the iron-chelator free-radical scavenger desferrioxamine. Lindane elicits a dose-dependent enhancement of total oxygen uptake by the liver, which is largely inhibited by 0.55 mM desferrioxamine. Total desferrioxamine- sensitive oxygen consumption exhibits a maximal increase (213 per cent) at 60 mg of lindane kg-1 over control values and represents 21 per cent of the total oxygen consumption. At the different doses of lindane used, it was calculated that about 60 per cent of the total increase in oxygen uptake by the liver is accounted for by oxygen related to oxidative stress, probably utilized at different stages of the induced lipid peroxidative process.

Animals↗
PubMed1988

Liver and biliary levels of glutathione and thiobarbituric acid reactants after acute lindane intoxication.

The i.p. administration of 60 mg kg-1 body weight of lindane, the gamma-isomer of hexachlorocyclohexane, to fed rats led to an enhancement of hepatic lipid peroxidation after 24 h of treatment. This was evidenced by significant increases in the hepatic production and biliary release of thiobarbituric acid reactive substances, and in the biliary release of glutathione disulphide. Under these conditions, the content of cytochrome P450 was enhanced concomitantly with increases in the total microsomal oxygen uptake, superoxide radical generation and (+)-catechin (cyanid-3-ol) sensitive respiration. The glutathione status of hepatocytes was altered by lindane as the content and biliary release of glutathione disulphide was drastically augmented, leading to a decrease in the cellular and biliary GSH/GSSG ratios. It is suggested that lindane treatment leads to an induced oxidative capacity, which, in turn, alters the glutathione status of the liver tissue.

Animals↗
PubMed1988

Lindane-induced oxidative stress. I. Time course of changes in hepatic microsomal parameters, antioxidant enzymes, lipid peroxidative indices and morphological characteristics.

1. Lindane (60 mg/kg) administered orally to rats increased liver cytochrome P-450 content and superoxide radical (O2-.) generation 24 h after treatment, while formation of thiobarbituric acid reactants and NADPH/ADP-supported microsomal chemiluminescence were significantly increased 4 h after treatment. 2. Hepatic superoxide dismutase (SOD) and catalase decreased 6 h after lindane treatment and SOD/O2-. ratio progressively decreased during 4 to 24 h after lindane treatment. 3. Morphological evidence of hepatic cell injury after lindane treatment was seen at all times studied, and appeared to increase with time. 4. Lindane administration results in time-dependent oxidative stress in liver which involves an early component (4-6 h) related to the reductive metabolism of lindane, and a late component (24 h) associated with the induction of cytochrome P-450; the biochemical changes correlated with the observed morphological lesions.

Animals↗