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Exposure to low levels of hydrogen sulfide elevates circulating glucose in maternal rats a

L. J. Hayden , Helen Goeden

b c

& S. H. Roth

c

a

Department of Pharmacology and Therapeutics, Division of Toxicology , University of Calgary , Calgary, Alberta, T2N 4N1, Canada b

Health Risk Associates, 2030 Addison Street, Suite 510, Berkeley, CA, 94704 c

Department of Pharmacology and Therapeutics, Division of Toxicology , University of Calgary , Calgary, Alberta, Canada Published online: 20 Oct 2009.

To cite this article: L. J. Hayden , Helen Goeden & S. H. Roth (1990) Exposure to low levels of hydrogen sulfide elevates circulating glucose in maternal rats, Journal of Toxicology and Environmental Health: Current Issues, 31:1, 45-52, DOI: 10.1080/15287399009531436 To link to this article: http://dx.doi.org/10.1080/15287399009531436

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EXPOSURE TO LOW LEVELS OF HYDROGEN SULFIDE ELEVATES CIRCULATING GLUCOSE IN MATERNAL RATS L. J. Hayden, Helen Goeden, S. H. Roth

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Department of Pharmacology and Therapeutics, Division of Toxicology, University of Calgary, Calgary, Alberta, Canada

Although the lethal effect of hydrogen sulfide (H2S) has long been known, the results of exposure to low levels of H2S have not been well documented. Rat dams and pups were exposed to low levels of H2S ( 75 ppm) from d 1 of gestation until d 21 postpartum and analyzed for changes in circulating enzymatic activity and metabolites. Blood glucose was significantly elevated in maternal blood on d 21 postpartum at all exposure levels. This increase in glucose was accompanied by a possible decrease in serum triglyceride in the pups and in the dams on d 21 postpartum. There was no evidence of alterations in serum alkaline phosphatase, lactate dehydrogenase, or serum glutamate oxaloacetate transaminase.

INTRODUCTION Hydrogen sulfide (H2S) at high levels is a known lethal compound that inhibits cytochrome oxidase and other metal-containing biological compounds by binding to metal ions. H2S or the metabolic products of H2S can also disrupt critical disulfide bonds in essential cellular proteins, possibly causing rapid neurological dysfunction, respiratory paralysis, and, with time, a disruption of cellular metabolism (Beauchamp et al., 1984). Hydrogen sulfide has been reported to cause species- and tissuespecific changes in alkaline phosphatase, acid phosphatase, adenosine triphosphate, and succinate dehydrogenase, an accumulative reduction of cerebral cytochrome oxidase, alterations in bile flow, and reduction in cerebral protein synthesis after acute exposure (Beauchamp et al., 1984; Elovoara et al., 1978). Other cellular constituents were also altered with a reduction in brain RNA, glutathione (Beauchamp et al., 1984), and a species-specific reduction of brain lipids at low levels of H2S (Gay et al., 1968). In the rabbit, 72 ppm H2S (30 min/d for 5 d) increased serum phosThe authors wish to thank H. Cheng, R. Bennington, and H. Mathison for technical assistance and V. Andrews for her typographic skills. This work was supported by Alberta Occupational Health and Safety: Heritage Fund. Present address for H. Goeden is Health Risk Associates, 2030 Addison Street, Suite 510, Berkeley, CA 94704. Requests for reprints should be sent to L. J. Hayden, Department of Pharmacology and Therapeutics, Division of Toxicology, University of Calgary, Calgary, Alberta T2N 4N1 Canada.

45 Journal of Toxicology and Environmental Health, 31:45-52, 1990 Copyright © 1990 by Hemisphere Publishing Corporation

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L. ] . HAYDEN ET AL.

phate while lowering alkaline phosphatase activity, serum copper, iron, and

Exposure to low levels of hydrogen sulfide elevates circulating glucose in maternal rats.

Although the lethal effect of hydrogen sulfide (H2S) has long been known, the results of exposure to low levels of H2S have not been well documented. ...
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