摘要:

AbstractDisulfiram, in 1 mg and 10 mg oral doses, was given to inbred C3H mice prior to and for the duration of pregnancy. The effects on the fetus have been assessed at 18 days gestation by means of fetal and placental weights, number of resorptions, skeletal preparations and Wilson's sections. Disulfiram dissolved in diethyl ether was administered to 8‐ and 9‐day embryosin vitroin concentrations of 0.1, 10 and 100 μgml−1of culture medium, and the effects of ether alone and ether plus disulfiram assessed by evaluation of morphological development over a 28‐h period, and inhibition of DNA synthesis using tritiated thymidine labelling over a 4‐h period. Disulfiram (1 mg)in vivocaused no adverse effects on the fetus, but disulfiram (10 mg) was toxic, in that it caused a significant increase in early resorptions. Disulfiramin vitro, in the 10 and 100 μg ml−1concentrations, proved to be very toxic to the embryos, affecting both morphological development and DNA synthesis in 9‐day embryos and morphological development in 8‐day embryos. DNA synthesis was only inhibited at the 100 μg ml−1concentration in 8‐day embryos. The 0.1 μg ml−1concentration of disulfiram caused abnormal central nervous system development in 8‐day embryos, but was otherwise non‐toxic to 8‐ and 9‐day embryos. Apart from a reduction in somite counts, ether in concentrations of 0.285 mg ml−1and 2.85 mg ml−1caused no adverse effects on morphological development in 8‐ or 9‐day embryos. DNA synthesis was inhibited by ether in a conc

ISSN:0260-437X    

DOI:10.1002/jat.2550050102

出版商:John Wiley&Sons, Ltd.    

年代:1985

数据来源: WILEY

摘要:

AbstractThe effect of different concentrations of fluoride (as sodium fluoride) on the enzymes lactate dehydrogenase (LDH, EC 1.1.1.27) and creatine kinase (CK, EC 2.7.3.2) in rabbit plasma was investigatedin vivoandin vitro. Rabbits were dosed orally, for 30 days, with fluoride at 2, 10 or 20 mg per kg body weight as sodium fluoride. LDH and CK levels were determined at 10‐day intervals during the treatment. Fluoride, depending on the applied dose, inhibited, had no effect or stimulated the investigated enzymesin vivo. On the other hand, fluoride had no effect on the activity of LDH and CKin vitr

ISSN:0260-437X    

DOI:10.1002/jat.2550050103

出版商:John Wiley&Sons, Ltd.    

年代:1985

数据来源: WILEY

摘要:

AbstractDeisopropylngaione (DIN) is one of a family of hepatotoxic furanosesquiterpenoid essential oils which is found in small amounts (5%) in the leaves of some specimens of the Australian plantMyoporum deserti. DIN differs from other furanoid myoporaceous essential oils in that it also causes lesions in the lungs and kidneys. At the near LD50dose rate of 150 mg kg−1given by intraperitoneal injection, DIN is able to cause lethal renal proximal tubular necrosis without causing significant injury to the liver and lungs in adult male mice. Following dosing, there is an increase in kidney weight due mainly to increase in water content which reaches a maximum within 16–24 h. This is accompanied by degeneration and necrosis of the proximal tubular epithelium, with proteinuria and glucosuria lasting up to 9 days in non‐lethally affected mice. Marked body weight loss due to the intoxication causes a marked increase in the kidney weight:body weight ratio lasting between 9 and 18 days. Residual lesions are still present in the kidneys at 32 days, but recovery is eventually complete. DIN is structurally similar to the sweet potato toxic furan 4‐ipomeanol and, like the latter, is probably injurious to the kidneys through toxic metabolism by the cytochrome‐P450‐containing monooxygenases of the proximal tubular epithelium. Although slight renal injury is occasionally observed in livestock poisoned by myoporaceous plants, it is unlikely that DIN is the cause. So far, DIN, like 4‐ipomeanol, appears to be unequivocally nephrotoxic only for t

ISSN:0260-437X    

DOI:10.1002/jat.2550050104

出版商:John Wiley&Sons, Ltd.    

年代:1985

数据来源: WILEY

摘要:

AbstractAdult male CD‐1 mice and CD rats were used to determine LD50/24 h lethality rates from exposure to 2450‐MHz circularly polarized microwaves. Groups of 16 mice or six rats were exposed in each of 32 combinations of nominal power density (10, 25, 50 or 75 mW cm−2), exposure duration (1 or 4 h), and environmental temperature (20 or 30 °C) and relative humidity (35 or 80%). An analysis of variance probit model was used to determine the influence each variable had on the probability of death. Significant factors in lethality were nominal power density, exposure duration and environmental temperature, but not environmental relative humidity. The estimated power density (mW cm−2) required to kill 50% of the animals in 24 h is halved when the environmental temperature is increased from 20 to 30 °C. Similarly, only 20–25% of the power density is required when the exposure duration is increased from 1 to 4 h. The use of nominal power density as a predictor of the probability of death was more efficient than specific absorption rate estimated experimentally by twin‐well calorimetry. The exposure of one mouse at a time, instead of 16, did not alter the predict

ISSN:0260-437X    

DOI:10.1002/jat.2550050105

出版商:John Wiley&Sons, Ltd.    

年代:1985

数据来源: WILEY

摘要:

AbstractThe capacity of thallium to substitute for K+in activation of (Na+, K+)‐ATPase of liver plasma membranes was studied. Our results indicate that Tl+can replace K+in the activation of the (Na+, K+)‐ATPase of liver plasma membranes. In the presence of Na+, similar activation is obtained with Tl+concentrations only 1/10 of those of K+. In all other aspects, the (Na+, K+)‐ and (Na+, Tl+)‐ATPases were found to be id

ISSN:0260-437X    

DOI:10.1002/jat.2550050106

出版商:John Wiley&Sons, Ltd.    

年代:1985

数据来源: WILEY

摘要:

AbstractThe effect of Mn2+, a divalent metal, on the enzyme K+‐p‐nitrophenyl phosphatase (K+‐PNPPase) was studied in rat brain. The metal was found to be a moderate inhibitor of the enzyme, with an I50of approximately 480 μM. The inhibition was pH dependent, but not temperature dependent. On measurement of the inhibition with varying concentrations of PNPP (1–5 mM), the I50value remained constant. However, when the inhibition was measured with K+(5–20 mM), the lso value increased from 130 μMto 490 μM, suggesting that K+antagonized the effect of Mn2+. In kinetic studies, Mn2+inhibited the enzyme in a non‐competitive manner with respect to PNPP. TheKmremained constant (2.9), but theFmaxwas decreased from 5.0 to 1.6. However, with respect to K+, the inhibition was competitive, as the concentration for half maximal activation (K0.5) increased from 1.3 to 8.9 mmol I−1with 1 mMof MnCl2, suggesting that the apparent affinity of K+for the enzyme was decreased. The apparentVmaxwas not affected. The degree of cooperativity (n) measured as the slope of the Hill plot remained unaltered (1.9 ± 0.2) over the entire concentration ran

ISSN:0260-437X    

DOI:10.1002/jat.2550050107

出版商:John Wiley&Sons, Ltd.    

年代:1985

数据来源: WILEY

摘要:

AbstractThe effect of exposure to chlorinated insecticides (DDT and toxaphene) on Na+, K+‐ATPase, Mg2+‐ATPase and Ca2+‐ATPase activities of the plasma membrane of hepatocytes was determined. Acute treatment with DDT (200 mg per kg body weight) or toxaphene (110 mg per kg body weight) produced a significant decrease in Na+, K+‐ATPase activity (80% and 85%, respectively) 24 h after treatment. DDT also produced a 30% decrease in Mg2+‐ATPase and Ca2+‐ATPase activity, but toxaphene treatment did not modify these enzymes. The effect of exposure to daily doses of DDT (30 mg per kg body weight) or toxaphene (16.5 mg per kg body weight) for a period of 3.5 months was also studied. Animals were sacrificed at 15‐day intervals and results showed that Na+, K+‐ATPase activity decreased 80% from the beginning of each treatment and the activity remained low throughout the treatment period. DDT, but not toxaphene, also led to a decrease in Mg2+‐ATPase (20%) and Ca2+‐ATPase (35%) activity. The low values observed from the beginning remained low throughout the treatment period. We believe that the general mechanism of ATPase inhibition by organochloride compounds could be the result of its interaction with membrane lipid components, although some differences could arise from differences in thei

ISSN:0260-437X    

DOI:10.1002/jat.2550050108

出版商:John Wiley&Sons, Ltd.    

年代:1985

数据来源: WILEY

摘要:

AbstractDimethyl sulfoxide (DMSO) was applied to a 2‐cm2area on the backs of four groups of mice for a 5‐min period each day, 5 days per week, for the designated periods: groups I and II — six hairless albino mice (hrhr, c/c) per group — were treated for 8 weeks; group III — three hairless albino mice (hrhr, c/c) — were treated for 4 weeks; group IV — three white mice (ICR Swiss) — were treated for 8 weeks. A group of six untreated hairless albino mice (hrhr, c/c) (group V) functioned as controls for groups I, II and III, and a group of three white mice (ICR Swiss) (group VI) served as controls for group IV. Except for DMSO applications, controls were handled and treated in the same way as the experimental groups. At the end of the experimental periods, the claws of all appendages were removed, measured and average lengths were determined. The claws of group I and group II hairless albino mice were, on average, 2.4‐fold longer than the claws of the control hairless albino mice, a significant increase (p<0.01) in the average claw length. There was no significant difference in the lengths of the claws of the group III mice after 4 weeks of DMSO application. The claws of group IV (ICR Swiss mice) were, on average, 1.2‐fold longer than the claws of the control white mice, representing a significant increase (p<0.02) in claw length after 8 weeks

ISSN:0260-437X    

DOI:10.1002/jat.2550050109

出版商:John Wiley&Sons, Ltd.    

年代:1985

数据来源: WILEY

ISSN:0260-437X    

DOI:10.1002/jat.2550050111

出版商:John Wiley&Sons, Ltd.    

年代:1985

数据来源: WILEY

ISSN:0260-437X    

DOI:10.1002/jat.2550050113

出版商:John Wiley&Sons, Ltd.    

年代:1985

数据来源: WILEY