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Eric A. Glende

Researcher at Case Western Reserve University

Publications -  35
Citations -  3469

Eric A. Glende is an academic researcher from Case Western Reserve University. The author has contributed to research in topics: Lipid peroxidation & Carbon tetrachloride. The author has an hindex of 21, co-authored 35 publications receiving 3416 citations.

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Journal ArticleDOI

Mechanisms of carbon tetrachloride toxicity

TL;DR: Le CCl 4 provoque une degenerescence lipidique et une necrose centrolobulaire du foie dans la peroxydation lipidique and les troubles hepatocellulaires de l'homeostase du calcium.
Book ChapterDOI

Spectrophotometric detection of lipid conjugated dienes.

TL;DR: Ultraviolet spectrophometric detection of conjugated dienes has been used for many years in the food industry for the detection of autoxidized lipids and for a variety of pathological processes, the question has been raised whether peroxidative decomposition of membrane lipids has occurred in vivo.
Journal ArticleDOI

Pathological mechanisms in carbon tetrachloride hepatotoxicity.

TL;DR: Data do not support the view that an increase in cytosolic free calcium is important in the toxic action of carbon tetrachloride or bromotrichloromethane, and carbon t trichlorometrichylperoxy-induced inhibition of very low density lipoprotein secretion by hepatocytes is not a result of elevated levels of cytosoli free calcium.
Journal ArticleDOI

Critical role of lipid peroxidation in carbon tetrachloride-induced loss of aminopyrine demethylase, cytochrome P-450 and glucose 6-phosphatase.

TL;DR: The experiments demonstrate conclusively that CCl 3 -Cl bond cleavage and covalent binding of products of CCl 4 metabolism do not constitute a mechanism for loss of microsomal glucose 6-phosphatase, cytochrome P-450 or aminopyrine demethylase for the particular anaerobic conditions employed in vitro.
Journal ArticleDOI

Carbon tetrachloride-induced protection against carbon tetrachloride toxicity. The role of the liver microsomal drug-metabolizing system.

TL;DR: The exact parallelism between depression of liver microsomal mixed function oxidase activity and resistance to the lethal effects of carbon tetrachloride affords strong evidence for the view that metabolism of CO2 by the livermicrosomal drug-metabolizing system is a necessary prerequisite for the toxicity of this liver poison.