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Biomedical subjects

N Konno

Publications and source records attributed to N Konno.

At least 73 records · Page 4Linked to original sources
PubMed1984

Lung injury and delayed toxicity produced by O,S,S-trimethyl phosphorodithioate, an impurity of malathion.

O,S,S,-Trimethyl phosphorodithioate (OSS-Me), an impurity present in organophosphorus insecticides, produced morphological alteration of rat and mouse terminal nonciliated bronchiolar epithelial (Clara) cells. The effects of OSS-Me on pulmonary and hepatic microsomal enzymes were studied following its po administration to rats. Oral 28-day LD50 of OSS-Me for rats was 67 mg/kg. The animals were treated with OSS-Me at 40, 100, and 160 mg/kg and killed 24 hr later. The relative lung weights were not affected at this time. Pulmonary microsomal benzo[a]pyrene hydroxylase decreased significantly; activities were less than 36% of control at the lowest dose. In contrast, the effect of OSS-Me treatment on hepatic monooxygenase activity was moderate. Benzo[a]pyrene hydroxylase, p-nitroanisole demethylase, or 7-ethoxycoumarin deethylase were not affected by OSS-Me treatment at any dose. Pulmonary and hepatic malathion carboxylesterase activities decreased following OSS-Me treatment. The decrease was more marked in liver. Time course effects of OSS-Me treatment on these parameters were examined by treating rats at 40 mg/kg, and the animals were killed at 6, 12, 24, and 72 hr after treatment. The lung relative wet weight was increased markedly at 72 hr. The benzo[a]pyrene hydroxylase activity of pulmonary microsomes was decreased at 24 and 72 hr after treatment, the maximum decrease being observed at 72 hr. At this time, glutathione of the lungs was depleted markedly. Significant decreases were not observed in hepatic monooxygenase activities. Liver glutathione content was not reduced at 72 hr. Pulmonary and hepatic malathion carboxylesterase activities decreased throughout the time course. OSS-Me selectively inhibited benzo[a]pyrene hydroxylase activity, depleted glutathione, and caused morphological alteration of Clara cells in lungs of rats. Although the toxic mechanism(s) produced by OSS-Me remains unknown, these results support the view that the lung is a target organ of OSS-Me-induced delayed toxicity.

Administration, Oral↗
PubMed1984

Protective effect of pretreatment against the acute toxicity of formulated cyanofenphos in hens.

Cyanofenphos (Surecide, O-ethyl O-4-cyanophenyl phenylphosphonothioate) is an organophosphorus pesticide. The protective effect against the near lethal dose, 140% the LD50, of formulated cyanofenphos developed in hens pretreated daily with a small dosage of 1.4% the LD50. The oral LD50 for formulated cyanofenphos was 700 mg/kg in the control hens and 1170 mg/kg in the hens pretreated with 10 mg/kg daily for 8 days. The length of the pretreatment period is important in inducing the protective effect. The protective action against 140% the LD50, 1,000 mg/kg, reached its maximum at approximately 24 hr after the last pretreatment. Pretreatment with 20 mg/kg daily for 8 days also acted as an antagonist for a challenge dose of 1,000 mg/kg. Three hours after a challenge dose of 400 mg/kg, brain acetylcholinesterase (AChE) activity was 0.14% delta pH/hr (17.6% of initial value) in hens pretreated with 10 mg/kg daily for 8 days and was 0.21 delta pH/hr (9.1% of initial value) in control hens, the difference being statistically significant (p less than 0.01). The protective effect of pretreatment against the acute toxicity of formulated cyanofenphos appears to be related to the fact that the formulation produced less inhibition of brain AChE activity in the pretreated hens than in the controls.

Acetylcholinesterase↗
PubMed1983

A comparison of measurements of serum free T3 concentration by equilibrium dialysis, free T3 index, and T3:TBG ratio in thyroidal and non-thyroidal illnesses.

The present study was undertaken and compare the methods for measuring free T3 (FT3) by equilibrium dialysis, free T3 index (FT3I), and T3:T4-binding globulin (T3/TBG) in 40 healthy subjects, 26 patients with hyperthyroidism, 36 patients with hypothyroidism, 16 women in the 3rd trimester of pregnancy, 5 euthyroid subjects with low TBG, and 24 patients with non-thyroidal illnesses (NTI) with normal or low serum T3 concentration. Both FT3I and T3/TBG correlated significantly with FT3 (r = 0.98, P less than 0.001 and r = 0.92, P less than 0.001, respectively) when the data from all subjects were analyzed together. When each group was analyzed separately, FT3I still correlated significantly with FT3 in all groups (r = 0.67-0.97) except in the NTIs with low T3 (r = 0.18). The correlation of T3/TBG with FT3 was also significant in all groups (r = 0.60-0.88) other than the euthyroid with low TBG (r = 0.32) and NTIs with low T3 (r = 0.04). Both FT3I and T3/TBG values agreed well with the FT3 level in hyper- and hypothyroid subjects. In euthyroidism with abnormal TBG level, FT3I agreed well with FT3. However, T3/TBG gave a falsely lower FT3 when the TBG level was high, and a falsely higher FT3 when the TBG was low. In NTIs with normal T3, both FT3I and T3/TBG agreed well with FT3, but FT3I and T3/TBG values were all subnormal in NTIs with low T3, where FT3 ranged from normal to subnormal. These data suggest that 1) both FT3I and T3/TBG may be equally useful for an assessment of FT3 level in hyper- and hypothyroidism, 2) FT3I may be superior to T3/TBG in euthyroidism with abnormal TBG concentration in serum, and 3) neither FT3I nor T3/TBG may be valid for an indirect measure of FT3 in NTIs with low serum concentration of T3.

Adult↗
PubMed1982

Seasonal variation of serum thyrotropin concentration and thyrotropin response to thyrotropin-releasing hormone in patients with primary hypothyroidism on constant replacement dosage of thyroxine.

Ten patients with primary hypothyroidism (aged 32--66 yr), replaced on constant daily doses of L-T4 (mean +/- SD, 1.90 +/- 0.22 micrograms/kg BW), were used to examine seasonal variations in serum levels of thyroid-related hormones for a period of 14 months. Basal and peak TSH concentrations after TRH (500 micrograms) were higher in winter than in summer. Summer values for basal TSH were all normal (normal range, less than 4.8 microU/ml), while winter values were supranormal in 5 of 10 patients. Summer values for peak TSH were subnormal or normal (normal range, 5.0--40.0 microU/ml), while winter values were supranormal in 3 patients, with the remaining values being normal [log basal TSH, 0.511 +/- 0.438 vs. 0.084 +/- 0.244 (P less than 0.05); log peak TSH, 1.394 +/- 0.410 vs. 1.017 +/- 0.423 (P less than 0.05)]. Serum resin T3 uptake, T4, free T4 index(FT4I), T3, free T3 index, and rT3 levels did not vary seasonally, although T4 and FT4I tended to fall in the winter. The summer and winter QKd interval (the interval from the onset of a QRS complex in the electrocardiogram to the appearance of the Korotkoff sound at diastolic pressure), basal metabolic rate, and serum cholesterol concentrations were all within the normal range. Basal and peak TSH after TRH were inversely correlated with serum T4 and FT4I levels. The basal TSH concentration was further inversely correlated with the seasonally altering ambient temperature. These results indicate that during the treatment of primary hypothyroidism with constant doses of T4, 1) serum TSH and its response to TRH show seasonal variation, 2) the hypersecretion TSH in the winter is related to small changes in serum T4 and FT4I levels, and 3) the seasonal variation in the serum TSH concentration may need to be taken into consideration when evaluating the adequacy of a T4 replacement dose.

Adult↗
PubMed1982

Delayed neurotoxicity resulting from administration of leptophos to the comb of domestic fowl.

We investigated the occurrence of delayed neurotoxicity in domestic fowl following percutaneous application of leptophos. Five groups of 5 adult hens received daily percutaneous doses of 1.0 ml/hen of leptophos emulsion (leptophos; 340 mg/hen/day) for 2, 5, 10, 15 or 20 days. There was no abnormal gait in the 2-day group. Two out of 5 hens in the 5-day group showed mild ataxia from about 2 weeks after the final administration, but did not develop severe neuropathy. On the contrary, 4 out of 5 birds in the 10-day group and all hens in the 15- and 20-day groups were affected by various stages of neurotoxicity. Some of them died from neurotoxicity. Ten of young male chickens were given the same dermal dose for 5 or 10 days. Although no abnormal chicken was observed in the 5-day group, all chickens in the 10-day group showed severe paralysis and two of them died. We studied the incidence rates of delayed neurotoxicity resulting from respective applications of the emulsion and the acetone solution of leptophos. No significant difference was observed between them. These results suggest that the daily dermal application of the relatively high dose of leptophos, even if for the short term, can cause the same delayed neurotoxic effects as by the oral administration in hens or chickens.

Animals↗
PubMed1980

[The maximum likelihood method for determining the normal range of thyrotropin concentration in human serum (author's transl)].

Radioimmunoassay techniques have been widely used for the measurement of serum thyrotropin concentrations. However, in spite of the great sensitivity of these techniques, some normal thyrotropin concentrations are still less than the minimum detectable amount. Data set in which contents below a fixed value are undetectable is referred to as Type 1 censored sample, and the maximum likelihood method can be applicable to define the normal range in this type of data. We have simultaneously measured serum thyrotropin concentrations obtained from 107 normal adult men by double antibody radioimmunoassay, and attempts were made to calculate the normal range by the maximum likelihood method. Distribution fitting of the censored data was determined by conventional chi-square tests, and it was found that the data fitted a normal log distribution. Although the serum thyrotropin concentration was undetectable (less than 0.625 microU/mL) in 14% of the subject, a normal range could be calculated. Using one-side tolerance limits for 95% coverage of the population with 90% confidence, we obtained the normal range of thyrotropin as 0.39 to 4.8 microU/mL with a mean value of 1.37 microU/mL, and predicted that 74.8% of undetectable thyrotropin values will fall within the normal range calculated above.

Adult↗