Oxidative injury and apoptosis of dorsal root ganglion neurons in chronic experimental diabetic neuropathy

Ann M. Schmeichel, James D. Schmelzer, Phillip Anson Low

Research output: Contribution to journalArticle

261 Citations (Scopus)

Abstract

We evaluated the effects of chronic hyperglycemia on L5 dorsal root ganglion (DRG) neurons using immunohistochemical and electrophysiologic techniques for evidence of oxidative injury. Experimental diabetic neuropathy was induced by streptozotocin. To evaluate the pathogenesis of the neuropathy, we studied peripheral nerve after 1, 3, and 12 months of diabetes. Electrophysiologic abnormalities were present from the first month and persisted over 12 months. 8-Hydroxy-2′-deoxyguanosine labeling was significantly increased at all time points in DRG neurons, indicating oxidative injury. Caspase-3 labeling was significantly increased at all three time points, indicating commitment to the efferent limb of the apoptotic pathway. Apoptosis was confirmed by a significant increase in the percentage of neurons undergoing apoptosis at 1 month (8%), 3 months (7%), and 12 months (11%). These findings support the concept that oxidative stress leads to oxidative injury of DRG neurons, with mitochondrium as a specific target, leading to impaired mitochondrial function and apoptosis, manifested clinically as a predominantly sensory neuropathy.

Original languageEnglish (US)
Pages (from-to)165-171
Number of pages7
JournalDiabetes
Volume52
Issue number1
DOIs
StatePublished - Jan 1 2003

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Diabetic Neuropathies
Spinal Ganglia
Apoptosis
Neurons
Wounds and Injuries
Streptozocin
Peripheral Nerves
Caspase 3
Hyperglycemia
Oxidative Stress
Extremities

ASJC Scopus subject areas

  • Internal Medicine
  • Endocrinology, Diabetes and Metabolism

Cite this

Oxidative injury and apoptosis of dorsal root ganglion neurons in chronic experimental diabetic neuropathy. / Schmeichel, Ann M.; Schmelzer, James D.; Low, Phillip Anson.

In: Diabetes, Vol. 52, No. 1, 01.01.2003, p. 165-171.

Research output: Contribution to journalArticle

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