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Biomedical subjects

B D Goldstein

Publications and source records attributed to B D Goldstein.

At least 109 records · Page 6Linked to original sources
PubMed1985

Acrylamide preferentially affects slowly adapting cutaneous mechanoreceptors.

Acrylamide (ACR) is a vinyl monomer which produces a distal axonopathy. Several investigators have shown that ACR produces deficits in proprioception. This deficit appears to result in part from altered muscle spindle function. ACR also produces deficits in cutaneous sensory perception. The purpose of these experiments was to determine whether ACR alters cutaneous sensory receptors. Cats were administered ACR (30 mg/kg) for either 3, 5, or 10 days. Following the last injection, the tibial nerve was isolated and four different mechanoreceptor types were isolated. These were field, rapid adapting (RA), and slowly adapting type 1 and type 2. The frequency response of the slowly adapting receptors was normal. However, the number of slowly adapting receptors identified was significantly reduced in all three ACR-treated groups. There was also a decrease in the number of field receptors after 10 day ACR administration. The total number of receptors per tibial nerve was unchanged in the ACR 3- and ACR 5-day groups but was significantly reduced in the ACR 10-day group. These data show a preferential effect of ACR on slowly adapting receptors early in the neuropathy. However, the reduction in field receptors and the total number of receptors at 10 days suggests that ACR eventually affects all mechanoreceptors in the tibial nerve.

Acrylamide↗
PubMed1985

Increase in substance P in the dorsal horn during a chemogenic nociceptive stimulus.

Substance P has been implicated as a neuromediator of nociception in the dorsal horn of the spinal cord. This is the first report of quantitative increases in substance P following an acute nociceptive stimulus. Female Wistar rats were injected subcutaneously in the plantar aspect of the right hindpaw with 5% formalin. Substance P levels were determined by quantitative immunohistochemistry 1 h after the injection. The present results show that substance P levels in the upper two laminae of the ipsi-and contralateral dorsal horn were significantly increased 1 h after the formalin injection. These results suggest a direct functional relationship between substance P levels in the upper dorsal horn and an acute chemogenic nociceptive stimulus.

Animals↗
PubMed1985

Acrylamide neurotoxicity: altered spinal monosynaptic responses to quipazine, a serotonin agonist, in cats.

The effects of the serotonin agonist quipazine on the spinal monosynaptic reflex (MSR) were investigated in acrylamide-treated cats. Cats were administered 30 mg/kg acrylamide (ACR) for 10 days, and the MSR and spontaneous ventral root discharge (VRD) were recorded on the tenth day (ACR 10) or 10 days subsequent to the last injection (ACR 20). Cumulative doses of quipazine were administered to increase the MSR and VRD. It was found that the MSR in ACR 10 cats was significantly depressed by ACR while the ACR 20 cats showed increased MSRs with double peaks. Dose-response relationships between quipazine and the area-under-the-MSR showed a significant shift to the right in the ACR 10 from control and no significant change in the ACR 20 from control. Dose-response curves of quipazine vs VRD showed no significant difference in either group from control. These data suggest that the alpha-motoneuron in ACR-treated cats was responding normally to quipazine while the primary afferent terminal was not.

Acrylamide↗
PubMed1985

Acrylamide alters oxidative enzyme activity in rat motoneurons.

Acrylamide (ACR) produces a central-peripheral distal axonopathy, via an unknown mechanism. We have investigated the effects of ACR on the activity of enzymes responsible for the oxidation of NADH (NADH-tetrazolium reductase activity, NADH-TR) with quantitative histochemical techniques. Chronic (5- or 10-day) injection of ACR (50 mg/kg/day) resulted in a significant decrease in enzyme activity in soleus motoneurons, which normally have high NADH-TR activity. The NADH-TR activity in motoneurons with low oxidative metabolism was not significantly affected. Retrograde labeling of motoneurons with horseradish peroxidase was diminished by the acrylamide treatment. These data demonstrate an acrylamide-induced change in the oxidative metabolism of certain motoneurons; further study will determine whether oxidative metabolism is the primary site of action of ACR in producing the distal axonopathy.

Acrylamide↗
PubMed1985

Muconaldehyde formation from 14C-benzene in a hydroxyl radical generating system.

It has recently been proposed that muconaldehyde, a six carbon, alpha, beta-unsaturated dialdehyde, may be a hematotoxic metabolite of benzene. The present studies indicate that trans, trans-muconaldehyde is formed from benzene in vitro in a hydroxyl radical (.OH) generating system containing ascorbate, ferrous sulfate and EDTA in phosphate buffer, pH 6.7. Muconaldehyde formed from benzene in the .OH generating system was identified by trapping it with thiobarbituric acid (TBA), which results in the formation of an adduct with a 495 nm absorption maximum and a 510 nm fluorescence emission maximum. These maxima were identical to those observed after reacting authentic trans, trans-muconaldehyde with TBA. This finding was supported by thin layer chromatography and solid phase extraction studies. In those studies benzene-derived muconaldehyde cochromatographed with the muconaldehyde/TBA standard. Analyses of the products from the .OH generating system using high performance liquid chromatography (HPLC) confirm that trans, trans-muconaldehyde is a product of benzene ring fission. Regardless of whether or not TBA was used for trapping, samples from the .OH system incubated with benzene contained a peak which cochromatographed with the muconaldehyde standard. The radioactivity profile of fractions collected during HPLC analysis demonstrates 14C-benzene to be the source of the trans, trans-muconaldehyde. The role of hydroxyl radicals in the formation of muconaldehyde was investigated by using dimethyl sulfoxide, mannitol, and ethanol as .OH scavengers. These scavengers, at concentrations of 10 and 100 mM, were found to cause a dose-dependent decrease in the formation of muconaldehyde.(ABSTRACT TRUNCATED AT 250 WORDS)

Aldehydes↗
PubMed1985

Investigations into the relations between respiratory illness in children, gas cooking and nitrogen dioxide in the U.K.

In 1977 an association was reported between the prevalence of respiratory illness and use of gas for cooking at home in a national sample of six to 11 year olds living in England and Scotland (p less than .10). Other variables such as social class and number of cigarette smokers at home did not seem to explain the association. As the gas cooker is an unflued appliance emitting a variety of pollutants during gas combustion it was suggested that indoor air pollution might explain the finding. Nitrogen dioxide (NO2) was suspected so a series of studies was conducted to investigate the distribution of levels of NO2 in the home, the relative contribution of sources of NO2 to indoor exposure and the relation between respiratory illness in six to 11 year olds and levels of NO2 in the home. The gas cooker was found to be one of the main sources of NO2 in the home. Winter weekly averages in kitchens with gas cookers had a mean of 112.2 ppb (n = 428, range 5-317 ppb). Levels in electric cooking kitchens were significantly lower (n = 87, mean 18 ppb, range 6-188 ppb). Studies of health indicated a relation between respiratory illness and bedroom levels of NO2 over the range 4-169 ppb (p .10). Results for living room levels of NO2 suggested a similar but non-significant relationship (p greater than .10). No relation was found for kitchen levels of NO2. For schoolchildren any effect on health from indoor NO2 is likely to be weak. However other sections of the population such as infants and the elderly who may spend more time indoors and are particularly susceptible to respiratory illness need to be studied to assess fully the impact that NO2 may be having on health.

Child↗
PubMed1984

Degradation of soluble collagen by ozone or hydroxyl radicals.

Collagen exposed to ozone or hydroxyl radicals was degraded in a time- and dose-dependent manner. This degradation was inhibited by free radical scavengers. Furthermore, lower levels of these oxidants did not degrade the molecule, but caused it to become susceptible to proteolytic degradation. We suggest an alternative mechanism by which oxygen-derived free radicals participate in the destruction of extracellular matrix observed during acute lung injury by oxidant gas, in addition to the commonly accepted proteinase-antiproteinase theory of lung injury.

Animals↗
PubMed1984

Evidence for hematotoxicity and tumorigenesis in rats exposed to 100 ppm benzene.

A group of 40 Sprague-Dawley rats was exposed to 100 ppm benzene for 6 h/day, 5 days/week for life. Another group of 40 rats received air under the same exposure regimen. During the exposures, treated rats exhibited continuously depressed peripheral erythrocyte and lymphocyte counts. Although the incidences of these peripheral cell depressions were statistically significant, the magnitudes of the depressions were not. Histopathologic evaluation revealed that splenic hemosiderin pigments were much more prevalent in exposed rats than in controls, indicating either red cell hemolysis or ineffective erythropoiesis. The mortality-corrected tumor incidences between exposed and control mice were not statistically different. However, several exposed rats died with tumors that, because of their rare spontaneous incidence, are most likely treatment-related. Four rats died with liver tumors, two died with zymbal gland carcinoma, and one died with chronic myelogenous leukemia.

Air Pollutants↗
PubMed1983

Neurotoxicology of vincristine in the cat. Morphological study.

Vincristine is a vinca alkaloid widely utilized in cancer chemotherapy. Its major clinical limitation is due to a drug induced sensory-motor neuropathy, the pathogenesis of which is poorly understood. This communication describes the morphological basis of a vincristine neuropathy in cats. Major pathological lesions were focal axonal swellings (giant axon formations) due to malaligned accumulations of neurofilaments and secondary demyelination of the paranodal type. These were primarily confined to the proximal portions of the peripheral nerves. The distal portions of the peripheral nerves contained only a few giant axon formations. Wallerian degeneration was noted to involve a small number of nerve fibers in the distal regions.

Animals↗
PubMed1983

Antinociception following microinjection of dibutyryl cyclic nucleotides into the caudal reticular formation and periaqueductal gray of the rat brain.

The tail flick, paw pinch, and hot plate tests were used to assess changes in nociceptive threshold following microinjection of dibutyryl derivatives of cyclic nucleotides into areas of the central nervous system previously shown to be involved in modulation of nociceptive threshold and mediation of morphine analgesia. An elevation in the nociceptive threshold was observed on all three tests following administration of 10 micrograms dibutyryl cyclic 3':5' adenosine monophosphate (db cAMP) into the caudal brainstem reticular formation (CRF) and periaqueductal gray (PAG). Two micrograms db cAMP produced the same magnitude of analgesia but had a shorter duration of action. Twenty micrograms dibutyryl cyclic 3':5' guanosine monophosphate (db cGMP) produced analgesia on all three tests following microinjection at CRF sites but not at PAG sites. These data indicate that morphine analgesia and the antinociception produced by cyclic nucleotides may involve, at least in part, common neuronal substrates. However, the observed capacity of db cAMP to elevate nociceptive threshold does not support the hypothesis that the mechanism of morphine's analgesic action involves inhibition of adenylate cyclase.

Analgesia↗
PubMed1982

Enhancement of rat and human phagocyte superoxide anion radical production by cadmium in vitro.

The mechanism by which cadmium produced oxidizing effects in vivo is unknown. We show that cadmium enhances the production of superoxide anion radical (O-(2) .), a reactive oxygen species, in digitonin-stimulated phagocytes from man and rat. Cadmium concentrations ranging from 3.6 X 10(-2)M to 3.6 X 10(-4)M inhibited O-(2) . production in rat alveolar macrophages or human granulocytes. However, when activated in the presence of 3.6 X 10(-5)M cadmium, the production of O-(2) . was increased by a factor of 2.11 +/- 0.25 above control levels in human granulocytes and 3.6 +/- 0.62 above control levels in rat alveolar macrophages. This effect by levels of cadmium within the range of those occurring during in vivo toxicity might provide an explanation for the oxidizing effects of this metal ion.

Animals↗
PubMed1982

Myelogenous leukemia in rodents inhaling benzene.

Studies during the past five decades have failed to demonstrate myelogenous leukemia in laboratory animals exposed to benzene despite epidemiologic evidence linking such exposure to myelogenous leukemia in man. We report four cases of myeloproliferative disease among rodents exposed to benzene, 6 h a day, 5 days weekly, for life. There was one case of chronic myelogenous leukemia, one of acute myeloblastic leukemia, and one of granulocytic hyperplasia among 40 CD-1 mice exposed to 300 ppm benzene; and one case of chronic myelogenous leukemia among 40 rats exposed to 100 ppm benzene. Although not statistically significant as compared to the respective control groups, the fact that myelogenous leukemia has not been reported in control animals of these two strains is suggestive of a causative role for benzene.

Animals↗
PubMed1982

Childhood respiratory illness and the home environment. I. Relations between nitrogen dioxide, temperature and relative humidity.

The relation between the use of gas for cooking, nitrogen dioxide (NO2), temperature and relative humidity was investigated in an urban area of northern England. In a pilot study conducted in a random sample of 40 homes measurements of temperature and relative humidity were not significantly different between homes with a gas cooker and homes with an electric cooker but weekly average levels of NO2 were higher in bedrooms (p less than 0.005) and living rooms (P less than 0.01) of gas homes. In the main study conducted in gas cooking homes only, access was gained to 183 (54.3%) of 337 randomly selected homes. No correlation was found in children's bedrooms between with weekly average level of NO2 (range 4.7 to 160.8 ppb) and weekly average temperature (ranged 7.7 to 22.0 degree C; r = 0.05, p greater than 0.10) or relative humidity (range 37.0 to 98.1%; r = 0.07, p greater than 0.10). Levels of NO2 in the bedroom were positively correlated with those in the living room (range 9.0 to 292.2 ppb; r = 0.39, p less than 0.01). Factors which tended to be associated with high levels of NO2 in the home included gas fires, paraffin heaters and use of the cooker for heating and drying clothes.

Air Pollutants↗