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R C Knight

Bio: R C Knight is an academic researcher. The author has contributed to research in topics: Polarography & Cyclic voltammetry. The author has an hindex of 1, co-authored 1 publications receiving 12 citations.

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Journal ArticleDOI
01 Jan 1989
TL;DR: The electrochemical characteristics of nitrosochloramphenicol have been studied in aqueous buffer systems using direct current (d.c.) and differential pulse polarography, cyclic voltammetry and coulometric techniques and two reduction mechanisms are discussed.
Abstract: The electrochemical characteristics of nitrosochloramphenicol have been studied in aqueous buffer systems (pH 7.1) using direct current (d.c.) and differential pulse polarography, cyclic voltammetry and coulometric techniques. Up to 4 charge-transfer steps can be identified. The first reduction step is reversible both chemically and electrochemically, the charge-transfer product showing no tendency to undergo further reaction on the electrochemical time-scale. In contrast, the second reduction step is irreversible, with the product undergoing a fast following reaction to yield a redox-active species which was detected by cyclic voltammetry. From the data and by comparison with related systems, two reduction mechanisms are possible and are discussed.

12 citations


Cited by
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Journal ArticleDOI
TL;DR: The mode of action, clinical application, and possible mutagenic action of nitroaromatic compounds is summarized.
Abstract: 1. Nitroaromatic compounds are important chemotherapy agents. 2. Their selective toxicity is determined by reduction to the biologically active form in the absence of oxygen. 3. Nitroaromatics are extensively used in the treatment of anaerobic infections and to target hypoxic tumor cells in cancer therapy. 4. Possible mutagenic action is related to the relative ease of nitro group reduction. 5. The mode of action and clinical application of nitroaromatic compounds is summarized.

97 citations

Journal ArticleDOI
TL;DR: In this paper, the cyclic voltammetry technique has been employed to study the tendency of nimodipine to undergo further chemical reactions, a dismutation reaction which is initiated electrochemically.

38 citations

Journal ArticleDOI
TL;DR: This is the first report of apoptosis in chloramphenicol toxicity and suggests a possible link between a metabolic event i.e. the production of free radicals; a morphological effect, apoptosis; and a clinical effect, bone marrow suppression and aplastic anaemia.
Abstract: 1 Chloramphenicol is used extensively in non-industrialized countries for the treatment of life-threatening infections because it is cheap and effective, despite its known hemotoxicity and linkage to fatal aplastic anaemia. It is important to define the mechanism of toxicity so that means can be devised to ameliorate the toxic effects in order to produce safer usage. 2 Chloramphenicol, at concentrations from 5 mM to 2 mM initiated apoptosis in dividing cells from a monkey kidney-derived cell line and in haematopoietic progenitor cells from human neonatal cord blood. 3 Growth of progenitor cells was suppressed at concentrations of chloramphenicol which would be considered less than therapeutic during patient treatment. 4 These effects could be ameliorated in progenitor cells by co-culture with the antioxidant mercaptoethylamine and in monkey kidney cells by co-culture with vitamin C. 5 This is the first report of apoptosis in chloramphenicol toxicity and suggests a possible link between a metabolic event i.e. the production of free radicals; a morphological effect, apoptosis; and a clinical effect, bone marrow suppression and aplastic anaemia.

32 citations

Journal ArticleDOI
TL;DR: This study examined whether the chloramphenicol enhancement of deafferentation‐induced cell death reveals the same ultrastructural characteristics that are seen in degenerating nucleus magnocellularis neurons after cochlea removal alone.
Abstract: Following cochlea removal in developing chicks, about 30% of the neurons in the ipsilateral second-order auditory nucleus, nucleus magnocellularis, undergo cell death. Administration of chloramphenicol, a mitochondrial protein synthesis inhibitor, results in a pronounced increase in deafferentation-induced cell death. In this study, we examined whether the chloramphenicol enhancement of deafferentation-induced cell death reveals the same ultrastructural characteristics that are seen in degenerating nucleus magnocellularis neurons after cochlea removal alone. Unilateral cochlea removal was performed on anaesthetized posthatch chicks. One group of animals was simultaneously treated with chloramphenicol. Six, twelve, or twenty-four hours following cochlea removal, n. magnocellularis neurons were studied by routine transmission electron microscopy. Particular attention was paid to the integrity of the polyribosomes and rough endoplasmic reticulum. Two ultrastructurally different types of neuronal degeneration were observed in the deafferented nucleus magnocellularis neurons: an early onset electron-lucent type that always involved ribosomal dissociation and a late-onset electron-dense type displaying nuclear pyknosis and severely damaged mitochondria. The percentage of nucleus magnocellularis neurons displaying ribosomal disintegration following cochlea removal was found to be markedly increased after chloramphenicol treatment. This finding suggests that mitochondrial function is important for the maintenance of a functional protein synthesis apparatus following deafferentation. © 1996 Wiley-Liss, Inc.

21 citations