Efficacy of N-Acetylcysteine in Treatment of Overt Diabetic Nephropathy
Status:
Completed
Trial end date:
2007-06-01
Target enrollment:
Participant gender:
Summary
Diabetic nephropathy has become the single most frequent cause of end-stage renal disease.
On a molecular level, at least five major pathways have been implicated in glucose-mediated
vascular and renal damage and all of these could reflect a single hyperglycaemia-induced
process of overproduction of reactive oxygen species.
Recent studies have shown that inflammation, and more specifically pro-inflammatory cytokines
play a determinant role in the development of micro- vascular diabetic complications, most of
the attention has been focused on the implications of TNF-α in the setting of diabetic
nephropathy.
Glutathione is the most abundant low-molecular-weight thiol, and Glutathione/ glutathione
disulfide is the major redox couple in animal cells.
N-acetylcysteine is effective precursors of cysteine for tissue Glutathione synthesis.
Not only does N-acetylcysteine exhibit antioxidant properties, but it may also counteract the
glycation cascade through the inhibition of oxidation.
N-acetylcysteine can also reduce the apoptosis elicited by reactive oxygen species .
Indeed, N-acetylcysteine has been shown to inhibit reactive oxygen species induced mesangial
apoptosis and to be able to protect cells from glucose-induced inhibition of proliferation.