Differential deoxyadenosine toxicity to immature rabbit cartilage in vitro. a model for the chondro‐osseous dysplasia of adenosine deaminase deficiency

Robert L. Wortmann; Judith A. Veum; Lawrence M. Ryan; Herman S. Cheung

doi:10.1002/anr.1780320811

Differential deoxyadenosine toxicity to immature rabbit cartilage in vitro. a model for the chondro‐osseous dysplasia of adenosine deaminase deficiency

Robert L. Wortmann, Judith A. Veum, Lawrence M. Ryan, Herman S. Cheung

Research output: Contribution to journal › Article › peer-review

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Abstract

Deoxyadenosine metabolism was investigated in rabbit growth plate and articular cartilage to elucidate the biochemical basis for the chondro-osseous dysplasia observed in adenosine deaminase (ADA) deficiency. Models of ADA deficiency, the combination of deoxyadenosine and either of 2 ADA inhibitors, were selectively toxic to immature cartilage, supporting the hypothesis that the chondro-ossoeus dysplasia of ADA deficiency is the consequence of the enzyme deficiency. Depletion of ATP may play a role in the altered chondrocyte viability and function observed in this model.

Original language	English (US)
Pages (from-to)	1014-1021
Number of pages	8
Journal	Arthritis & Rheumatism
Volume	32
Issue number	8
DOIs	https://doi.org/10.1002/anr.1780320811
State	Published - Aug 1989
Externally published	Yes

ASJC Scopus subject areas

Immunology and Allergy
Rheumatology
Immunology
Pharmacology (medical)

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abstract = "Deoxyadenosine metabolism was investigated in rabbit growth plate and articular cartilage to elucidate the biochemical basis for the chondro-osseous dysplasia observed in adenosine deaminase (ADA) deficiency. Models of ADA deficiency, the combination of deoxyadenosine and either of 2 ADA inhibitors, were selectively toxic to immature cartilage, supporting the hypothesis that the chondro-ossoeus dysplasia of ADA deficiency is the consequence of the enzyme deficiency. Depletion of ATP may play a role in the altered chondrocyte viability and function observed in this model.",

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AU - Ryan, Lawrence M.

AU - Cheung, Herman S.

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AB - Deoxyadenosine metabolism was investigated in rabbit growth plate and articular cartilage to elucidate the biochemical basis for the chondro-osseous dysplasia observed in adenosine deaminase (ADA) deficiency. Models of ADA deficiency, the combination of deoxyadenosine and either of 2 ADA inhibitors, were selectively toxic to immature cartilage, supporting the hypothesis that the chondro-ossoeus dysplasia of ADA deficiency is the consequence of the enzyme deficiency. Depletion of ATP may play a role in the altered chondrocyte viability and function observed in this model.

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Differential deoxyadenosine toxicity to immature rabbit cartilage in vitro. a model for the chondro‐osseous dysplasia of adenosine deaminase deficiency

Abstract

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