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Taurine Replacement Prevents Apoptosis In Experimental Diabetic Neuropathy
Author(s) -
PopBusui R,
Sullivan K,
Russel J,
Feldman E,
Stockert C,
Larkin D,
Greene D,
Stevens M.
Publication year - 2000
Publication title -
journal of the peripheral nervous system
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1
H-Index - 67
eISSN - 1529-8027
pISSN - 1085-9489
DOI - 10.1046/j.1529-8027.2000abstracts-37.x
Subject(s) - taurine , oxidative stress , dorsal root ganglion , endocrinology , tunel assay , medicine , streptozotocin , diabetic neuropathy , apoptosis , diabetes mellitus , chemistry , anatomy , dorsum , biochemistry , immunohistochemistry , amino acid
The pathophysiology of diabetic neuropathy (DN) is complex involving both metabolic and vascular deficits. Recent data have implicated a potential role for programmed cell death (PCD) in the development of experimental DN (EDN). Oxidative stress has emerged as a leading candidate in the development of nerve blood flow (NBF) and nerve conduction deficits. We have previously shown that replacement of the endogenous antioxidant taurine in the nerve of streptozotocin‐diabetic (STZ‐D) rats corrects neuro‐vascular dysfunction, prevents deficits in Na,K‐ATPase activity and attenuates motor and sensory NCV slowing. The aims of this study were to examine the hypothesis that oxidative stress‐mediated mitochondrial dysfunction may promote the activation of PCD pathways in STZ‐D rats and to determine whether these effects could be attenuated by taurine. Dorsal root ganglion (DRG) neurons were extracted from perfused control (C), STZ‐D and STZ‐D rats given a 1% taurine supplemented diet for 6 weeks. STZ‐D induced a significant decrease in sensory nerve conduction velocity (SNCV) and NBF vs controls and these deficits were corrected by taurine. Lumbar and sacral DRG were sectioned at 10 mm intervals and slides were prepared from two different sampling sites. Apoptosis was detected by TUNEL staining. 150 or more DRG nuclei were counted per animal. In STZ‐D rats 21.3 ± 4.9% of DRG nuclei were found to be TUNEL positive as compared with 2.9 ± 2.1% in controls (p < 0.05). Taurine replacement markedly attenuated apoptosis since only 6.5 ± 2.9% neurons were TUNEL positive. In summary, 6 weeks of STZ‐D increased apoptosis in DRG neurons of STZ‐D rats. This increase in apoptosis could be prevented by replacement of the endogenous antioxidant taurine, implicating a role of taurine depletion in the development of sensory neuron degeneration.