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B Ballantyne

Publications and source records attributed to B Ballantyne.

17 recordsLinked to original sources
PubMed1979

Comparison of kinetic and end-point microdensitometry for the direct quantitative histochemical assessment of cytochrome oxidase activity.

Cytochrome oxidase activity has been assessed by a method of kinetic microdensitometry which involves applying tissue sections to gel films containing phenylamine substrates and measuring the rate of azine dye production by continuously recording the rate of change in extinction. Optimum conditions for the technique were defined, and the results compared with those obtained by conventional end-point microdensitometry in which sections are incubated in histochemical substrate solutions and azine dye production estimated by a single measurement of extinction at the end of the incubation period. When compared with biochemically-determined enzyme activity, kinetic microdensitometry gave a better index of the proportionate activity of cytochrome oxidase in various normal tissues than did end-point microdensitometry. In addition, the degree of inhibition of cytochrome oxidase activity in tissues removed from cyanide-poisoned animals was assessed more reliably by kinetic microdensitometry than by end-point measurements. With end-point microdensitometry, the reaction is non-linear over the comparatively long incubation times required and there is also a spontaneous reactivation of cyanide-inhibited cytochrome oxidase during incubation and thus a progressively increased rate of substrate utilization. In contrast, with kinetic microdensitometry the initial linear reaction rate is measured before significant reactivation occurs. Kinetic microdensitometry can be used for direct dynamic quantitation of enzyme activity in tissues or cells; it may be a valuable technique for quantitative histochemical confirmation or extension of biochemical studies; and it appears to be a reliable direct quantitative histochemical method for investigating in vivo inhibition of enzyme activity, where spontaneous reactivation of the enzyme-inhibitor complex may occur.

Animals↗
PubMed1979

Blood cyanide.

Explore the source record for details and available documents.

Cyanides↗
PubMed1978

The comparative acute mammalian toxicity of 1-chloroacetophenone (CN) and 2-chlorobenzylidene malononitrile (CS).

The comparative acute toxicity of two peripheral sensory irritant materials, 1-chloroacetophenone (CN) and 2-chlorobenzylidene malononitrile (CS), has been investigated in several species of small mammal using solutions in polyethylene glycol 300 for intravenous, intraperitoneal and oral administration, and as pure aerosols for inhalation exposure. Additionally, the comparative potency for inducing primary contact dermatitis was studied. CN and CS were found to be about equitoxic by intravenous and intraperitoneal injection, but CS was significantly less toxic by the oral and inhalation routes and less likely to cause non-lethal tissue damage than CN.

Administration, Oral↗
PubMed1978

The comparative short-term mammalian toxicology of phenarsazine oxide and phenoxarsine oxide.

Phenoxarsine oxide (PXO) and phenarsazine oxide (PZO) are organic arsenicals used as industrial biocides. The acute LD50 (in mg kg-1) for PZO was 83 (rat) and 77 (guinea pig) and for PXO 40 (rat) and 24 (guinea pig). PXO was more irritant to the gastrointestinal tract. Liver pathology did not occur in PZO-guinea pigs, but PZO was more hepatotoxic than PXO in rats. The acute inhalation L (ct)50 values were 12830 mg min m-3 for PXO and 13650 mg min m-3 for PZO in guinea pigs; death was due to asphyxia. The guinea pig acute L(ct)50 given as a divided dose over 30 days to guinea pigs and rats did not produce toxic signs, but mononuclear cell infiltration of the portal tracts occurred. PXO and PZO were found to be primary skin and eye irritants; PXO produced more severe effects. The no-effect concentration for keratitis with solutions was 0.25% PZO and 0.1% PXO; both compounds caused concentration dependant transient increases in intraocular pressure, the proportionate increases being significantly greater with PXO. Thus, although PXO and PZO are equitoxic by acute inhalation, PXO is more toxic orally and more irritant to the skin, eye and gastrointestinal tract but PZO is more hepatotoxic.

Administration, Oral↗
PubMed1978

Neuronal and non-neuronal choline ester hydrolases in the rabbit liver.

Biochemical and histochemical methods have been used to determine both activity and distribution of choline ester hydrolases in the rabbit liver. Acetylcholinesterase was detected in kupffer cells, predominantly in th centri- and mid-lobular regions. Neither the activity nor the distribution of acetylcholinesterase activity was influenced by the intravenous injection of zymosan or the iron-dextran complex imferon on at dosages known to stimulate reticuloendothelial phagocytic function. Although this finding suggests that acetylcholinesterase is not primarily concerned with the pocesses of phagocytosis, there exists the possibility that reticuloendothelial acetylcholinesterase may have a function in metabolism of phagocytosed lipids and esters. Butyrylcholinesterase was present in both hepatocytes and the intrinsic hepatic nerves. Polarization of hepatocyte butyrylcholinesterase activity was noted; the enzyme activity being most marked in the centrilobular hepatocytes. Hepatocyte butyrylcholinesterase activity was unaffected by the intravenous administration of zymosan or imferon. The intrinsic hepatic nerves were present only in portal tracts and interlobular septa, there being no evidence for the existence of an hepatic parenchymal plexus. These findings by cholinesterase histochemistry were confirmed by controlled neurohistological techniques. The morphological findings suggest that the intrinsic hepatic nerves regulate blood flow through the organ and are possible sensory to the bile ducts.

Acetylcholinesterase↗
PubMed1977

The acute mammalian toxicology of dibenz(b,f)-1,4-oxazepine.

Dibenz(b,f)-1,4-oxazepine (CR), a potent peripheral sensory irritant material, has been shown to have a very low acute lethal and sub-lethal toxicity by intravenous, intraperitoneal, oral, percutaneous and inhalation routes to several species of laboratory mammal. There was no organ-specific pathology. Comparison of the acute toxicity of CR with that of two other peripheral sensory irritants, 1-chloroacetophenone (CN) and 2-chlorobenzyl-lidene malononitrile (CS), shows CR to be significantly less toxic than either of them. Pyrotechnically generated CR smoke was more toxic than pure (thermally generated) aerosols of CR; this was due to the presence of pyrotechnic decomposition products in the atmosphere from the burning of the smoke generating composition. However, the median lethal toxicity of pyrotechnically generated CR smoke was very significantly less than that of either pyrotechnically generated CN or CS smokes. Short-term cumulative toxicity did not occur following multiple oral dosing with CR. The acute toxicology of three ether intermediates encountered in the synthesis of CR from 1-chloro-2-nitrobenzene and sodium phenoxide (2-nitrodiphenyl ether, 2-aminodiphenyl ether and 2-formamidodiphenyl ether) was investigated; all three ethers were found to be less acutely toxic than CR itself.

Administration, Oral↗
PubMed1977

In vitro production of cyanide in normal human blood and the influence of thiocyanate and storage temperature.

Normal human blood stored at room temperature (about 20 degrees C) may, over a period of weeks, undergo a slow transformation of its cyanide content. In contrast, when normal blood is stored at -20 degrees C there is formation of cyanide, usually occurring most rapidly during the first few days of storage. Peak concentrations are never greater than 20 microgram/100 ml, and although some fluctuation in concentration occurs over several months of storage at deep freeze temperature, levels are always higher than in the freshly drawn blood. The amount of cyanide produced appears to be a function of both the initial thiocyanate concentration and the freezing and/or thawing of blood. Blood stored at refrigerator temperature (about 4 degrees C) has the least fluctuation in cyanide concentration over a storage period up to three months. During this study it was found that there is significant difference in whole blood cyanide concentration between smokers and nonsmokers.

Adult↗
PubMedDate not supplied

The ophthalmic toxicology of dichlorøomethane.

The toxic hazard to the eye from dichloromethane (DCM) as liquid or vapour has been assessed rabbits. 0.1 ml DCM caused inflammation of the conjunctiva and eyelids persisting for up to 2 weeks; keratitis and iritis occurred in two-thirds of the animals. Corneal thickness, measured in vivo, increased by a maximum of 59% at 6 h, returning to normal by 9 days. 0.01 ml DCM produced similar, but less persistent effects on the conjunctiva and eyelids; keratitis was minor. Corneal thickness increased by up to 43% at 6 h, returning to normal by 9 days. Intraocular tension increased by 33% at 1 h, returning to control values by 3 days. 10-min exposures to DCM vapour at concentrations up to 17 500 mg/m3 produced no macroscopic changes, but small increases in corneal thickness and intraocular tension occurred, which were related to the degree of exposure. The mean peak increases in corneal thickness were 13% for 17 500 mg/m3 and 5% for 1750 mg/m3; corresponding values for increases in intraocular tension were 18% and 11%. Both corneal thickness and intraocular tension returned to normal by 2 days. Treatment with a decongestant preparation (Vasocon-A), containing an antihistamine and an alpha-adrenergic sympathomimetic, reduced both the inflammatory response and the rise in intraocular pressure caused by a splash contamination of the eye with liquid DCM.

Animals↗