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Unimpaired energy metabolism in experimental neuropathy induced by p‐bromophenylacetylurea
Author(s) -
Brimijoin Stephen,
Mintz Keith P.
Publication year - 1984
Publication title -
muscle and nerve
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.025
H-Index - 145
eISSN - 1097-4598
pISSN - 0148-639X
DOI - 10.1002/mus.880070906
Subject(s) - glycolysis , phosphofructokinase , medicine , endocrinology , glyceraldehyde 3 phosphate dehydrogenase , adenosine triphosphate , hindlimb , oxidative phosphorylation , creatine , high energy phosphate , sciatic nerve , phosphofructokinase 1 , enolase , metabolism , chemistry , phosphocreatine , biology , biochemistry , energy metabolism , dehydrogenase , enzyme , immunohistochemistry
The contribution of defective energy metabolism to the induction of neuronal pathology by p‐bromophenylacetylurea (BPAU) was examined in several ways. It was found that a saturated aqueous solution of BPAU had no effect on the activity of crystalline glyceraldehyde‐3‐phosphate dehydrogenase (GAPDH) or phosphofructokinase (PFK). In rats with total hindlimb paralysis from treatment with BPAU (400 mg/kg), the endogenous GAPDH and PFK of sciatic nerve showed normal activity. Endogenous enolase and nerve‐specific enolase activities were likewise unaffected. Consequently, it appeared improbable that BPAU neuropathy involves impaired glycolysis. This conclusion was supported by the failure to prevent hindlimb weakness by feeding pyruvate, a substrate for the Krebs cycle. To test for interference with glycolysis at other steps, or for an impairment in oxidative phosphorylation, adenosine triphosphate (ATP) and creatine phosphate were measured. The amounts of high energy phosphates in nerves of paralyzed animals were found to be the same as in nerves of untreated and vehicle‐treated controls. A similar observation was made in nerves regenerating from a crush injury. To test turnover, ATP and creatine phosphate were measured in nerves exposed to an N 2 atmosphere in vitro. Since the high energy phosphates disappeared at the same rates in all groups, it was concluded that BPAU neuropathy does not alter energy utilization. In our view, BPAU neuropathy arises by a mechanism that does not depend on altered energy metabolism.