Boron, boric acid, borates and boron oxide.
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Biomedical subjects
Publications and source records attributed to R Von Burg.
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Like most organic solvents, xylene has irritating effects on the skin, mucous membranes and respiratory tract. It has a narcotic effect on the nervous system, variable effects on the liver and kidneys, and questionable effects on the cardiovascular system and female reproductive system. Xylene was thought to be deleterious to the hemopoietic system, but more recent studies concluded that such effects were due to benzene contamination or inflammation response to xylene injection. The latest evidence indicates that xylenes are not co-carcinogenic, carcinogenic or teratogenic. If maternal toxicity is avoided, xylenes do not have embryotoxic effects.
The development of acrylamide induced neurotoxicity was followed for 3 weeks in the mouse by behavioral testing, determination of conduction velocities and electron microscopic examination of peripheral nerves. Neurotoxic signs began to appear during the second week of treatment. A condition of severe intoxication developed within 21 days. Behavioral assessment for neurological deficits proved to be more sensitive than sensory or motor conduction velocity determinations either in isolated preparations or in situ. In general, such electrophysiological determinations did not result in reproducible, statistically significant, differences from control animals until the third week of acrylamide administration. However, there was a suggestion that temperature reduction may provide a provocative change to increase the sensitivity of such electrophysiological measurements. Electron microscopic examination of the nerves of severely poisoned animals revealed myelin corrugation and delamination to be the most consistent damage. Acrylamide appeared to produce a nonselective attack since degenerating fibers were found intermingled with almost normal fibers of approximately the same diameter. In general, the production of neurotoxicity in the mouse closely resembled that seen in the rat but some differences were noted.
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I.p. administration at several dose levels over periods of up to 12 weeks, or continuous i.v. infusion of high doses of misonidazole (MISO) for 15 h, produced no significant change in peripheral nerve conduction velocity (NCV) and did not prevent the normal increase in NCV as the animals matured from 12 to 24 weeks of age. Peripheral NCV (sural nerve) was reduced in both MISO-treated and control mice with hind-limb tumour implants, presumably owing to physical pressure due to tumour growth. In addition, neither the medial nerves nor the tibial nerve in the normal limbs of the tumour-implanted, drug-treated animals showed any change. Consequently our earlier and present studies do not confirm the recent reports of changes in NCV following either acute or chronic MISO administration to mice.
No effective therapeutic agent for mobilizing tissue Cd has been reported to date, but the results presented here demonstrate that 2,3-dimercaptopropanol (BAL) , at doses approaching and surpassing the maximum tolerated, can produce a rapid transient enhancement of Cd excretion in the rat. When BAL (75 mg/kg) was administered by a single injection 24 h after a tracer dose of 109Cd, as much as 32% of the administered Cd appeared in the bile. A correlation between the appearance of radiocadmium and the biliary sulfhydryl concentration was found. There was indirect evidence for a 1:3 Cd-BAL complex in the bile, which may explain the efficacy of higher doses of BAL. A comparative study with some selected dithiol compounds suggests that vicinal sulfhydryl groups on an aliphatic chain are the more effective Cd mobilizing compounds, but BAL was the most effective agent. Although suspending vehicles alone showed no Cd mobilizing ability, the combination of BAL and oil was far superior to any other BAL-vehicle combination used. A spectrophotometric method for the determination of sulfhydryl groups in bile and urine is also presented.
Contrary to an earlier report that metronidazole exhibited anticholinesterase activity on isolated organ preparations, a direct spectrophotometric assay was unable to demonstrate any significant inhibition of either true or pseudocholinesterase activity in the presence of this drug. The related nitroimidazole, misonidazole, was also found to be inactive when tested in this system. This report demonstrates that the clinical neurotoxicity of these two compounds cannot be attributed to any direct effect on the cholinesterase enzymes.
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The clinical use of the radiosensitizer misonidazole may be limited by the incidence of peripheral neuropathy reported following total doses in excess of 18 g. A recent report noted a decrease in nerve conduction velocity following a single i.p. injection of 1 mg/g misonidazole in mice. The present study was unable to confirm such changes when nerve conduction velocity measurements were made in situ or in isolated sural, tibial or median nerves of mice. Other electrophysiological parameters such as threshold, strength-duration curves, refractory time or the ability to carry high-frequency stimulation also showed no change. However, it was noted that a single administration of the radio-sensitizer produced a marked decrease in body temperature which persisted for at least 2 h after the elimination of the drug from the blood serum. The physiological response of reduction of body temperature may protect the mouse against the effect of the toxic chemical species involved in the induction of neurotoxicity.