Effectiveness of N-acetylcysteine in protecting against mercuric chloride-induced nephrotoxicity

Glutathione Monoethyl Ester Moderates Mercuric Chloride-Induced Acute Renal Failure

“…It is specula tive as to whether a larger dose of GE would prevent cellular injury following MC although we suspect not, as in vitro studies using rabbit proximal tubular epithelial cells in culture suggest that the pathogenesis of cellular injury fol lowing M exposure involves more than an interaction with thiol groups [40]. The effects of GE noted in our study confirm the preliminary observations of Naganuma et al [33] and are similar to those previously reported for DTT [13,14,35], N-acetylcysteine [13] and captopril [16]. Of interest, the protection associated with DTT treatment occurs in the absence of any change in M accumulation within the total kidney [14] or renal cortex [15] and even though it does not restore renal sulfhydryl status or the activity of Mg-or Na, K-ATPase [41].…”

“…Previous studies that we [11] and others [12] have conducted, demonstrate that GSH depletion selectively reduces mercury accumulation within the kidney, but increases mortality following MC. However, these observations are contrary to the recent report of Girardi and Elias [13], who reported that GSH depletion increased renal M accumulation and augmented nephrotoxicity. We [11] have also suggested that MC ne phrotoxicity is enhanced following GSH depletion, al though Johnson [12] noted a moderation of MC-induced tubular dysfunction in this circumstance.…”

Glutathione Monoethyl Ester Moderates Mercuric Chloride-Induced Acute Renal Failure

“…It is specula tive as to whether a larger dose of GE would prevent cellular injury following MC although we suspect not, as in vitro studies using rabbit proximal tubular epithelial cells in culture suggest that the pathogenesis of cellular injury fol lowing M exposure involves more than an interaction with thiol groups [40]. The effects of GE noted in our study confirm the preliminary observations of Naganuma et al [33] and are similar to those previously reported for DTT [13,14,35], N-acetylcysteine [13] and captopril [16]. Of interest, the protection associated with DTT treatment occurs in the absence of any change in M accumulation within the total kidney [14] or renal cortex [15] and even though it does not restore renal sulfhydryl status or the activity of Mg-or Na, K-ATPase [41].…”

“…Previous studies that we [11] and others [12] have conducted, demonstrate that GSH depletion selectively reduces mercury accumulation within the kidney, but increases mortality following MC. However, these observations are contrary to the recent report of Girardi and Elias [13], who reported that GSH depletion increased renal M accumulation and augmented nephrotoxicity. We [11] have also suggested that MC ne phrotoxicity is enhanced following GSH depletion, al though Johnson [12] noted a moderation of MC-induced tubular dysfunction in this circumstance.…”

Glomerular compromise in mercuric chloride-induced nephrotoxicity

“…Moreover, inflammatory cells release eicosanoids and reactive oxygen metabolites. The release of such substances was previously described in HgCl 2 -treated animals (4), and the substances were proposed as contributors in the glomerular structural and functional damage (3,4). Present results describe higher accumulation of lipids in renal sections, principally in glomeruli areas, and this phenomena could be taken also as the result of an inflammatory process.…”

The Effect of N-Acetylcysteine on Proteinuria and Markers of Tubular Injury in Non-Diabetic Patients with Chronic Kidney Disease

“…Some reports [37] , but not all [38] , have shown that it can inhibit NF-B activation in renal mesangial and epithelial cells. Interventional animal studies have confirmed the nephroprotective properties of NAC in cyclosporine-and mercury-induced nephrotoxicity as well as in ischemia/ reperfusion injury [39][40][41][42] . The attenuation of histological abnormalities involving tubular injury as well as preservation of renal function were observed after NAC.…”

Glutathione Monoethyl Ester Moderates Mercuric Chloride-Induced Acute Renal Failure

“…It is specula tive as to whether a larger dose of GE would prevent cellular injury following MC although we suspect not, as in vitro studies using rabbit proximal tubular epithelial cells in culture suggest that the pathogenesis of cellular injury fol lowing M exposure involves more than an interaction with thiol groups [40]. The effects of GE noted in our study confirm the preliminary observations of Naganuma et al [33] and are similar to those previously reported for DTT [13,14,35], N-acetylcysteine [13] and captopril [16]. Of interest, the protection associated with DTT treatment occurs in the absence of any change in M accumulation within the total kidney [14] or renal cortex [15] and even though it does not restore renal sulfhydryl status or the activity of Mg-or Na, K-ATPase [41].…”

“…Previous studies that we [11] and others [12] have conducted, demonstrate that GSH depletion selectively reduces mercury accumulation within the kidney, but increases mortality following MC. However, these observations are contrary to the recent report of Girardi and Elias [13], who reported that GSH depletion increased renal M accumulation and augmented nephrotoxicity. We [11] have also suggested that MC ne phrotoxicity is enhanced following GSH depletion, al though Johnson [12] noted a moderation of MC-induced tubular dysfunction in this circumstance.…”

Glomerular compromise in mercuric chloride-induced nephrotoxicity

“…Moreover, inflammatory cells release eicosanoids and reactive oxygen metabolites. The release of such substances was previously described in HgCl 2 -treated animals (4), and the substances were proposed as contributors in the glomerular structural and functional damage (3,4). Present results describe higher accumulation of lipids in renal sections, principally in glomeruli areas, and this phenomena could be taken also as the result of an inflammatory process.…”

The Effect of N-Acetylcysteine on Proteinuria and Markers of Tubular Injury in Non-Diabetic Patients with Chronic Kidney Disease

“…Some reports [37] , but not all [38] , have shown that it can inhibit NF-B activation in renal mesangial and epithelial cells. Interventional animal studies have confirmed the nephroprotective properties of NAC in cyclosporine-and mercury-induced nephrotoxicity as well as in ischemia/ reperfusion injury [39][40][41][42] . The attenuation of histological abnormalities involving tubular injury as well as preservation of renal function were observed after NAC.…”

Glutathione Monoethyl Ester Moderates Mercuric Chloride-Induced Acute Renal Failure

“…It is specula tive as to whether a larger dose of GE would prevent cellular injury following MC although we suspect not, as in vitro studies using rabbit proximal tubular epithelial cells in culture suggest that the pathogenesis of cellular injury fol lowing M exposure involves more than an interaction with thiol groups [40]. The effects of GE noted in our study confirm the preliminary observations of Naganuma et al [33] and are similar to those previously reported for DTT [13,14,35], N-acetylcysteine [13] and captopril [16]. Of interest, the protection associated with DTT treatment occurs in the absence of any change in M accumulation within the total kidney [14] or renal cortex [15] and even though it does not restore renal sulfhydryl status or the activity of Mg-or Na, K-ATPase [41].…”

“…Previous studies that we [11] and others [12] have conducted, demonstrate that GSH depletion selectively reduces mercury accumulation within the kidney, but increases mortality following MC. However, these observations are contrary to the recent report of Girardi and Elias [13], who reported that GSH depletion increased renal M accumulation and augmented nephrotoxicity. We [11] have also suggested that MC ne phrotoxicity is enhanced following GSH depletion, al though Johnson [12] noted a moderation of MC-induced tubular dysfunction in this circumstance.…”

Glomerular compromise in mercuric chloride-induced nephrotoxicity

“…Moreover, inflammatory cells release eicosanoids and reactive oxygen metabolites. The release of such substances was previously described in HgCl 2 -treated animals (4), and the substances were proposed as contributors in the glomerular structural and functional damage (3,4). Present results describe higher accumulation of lipids in renal sections, principally in glomeruli areas, and this phenomena could be taken also as the result of an inflammatory process.…”

The Effect of N-Acetylcysteine on Proteinuria and Markers of Tubular Injury in Non-Diabetic Patients with Chronic Kidney Disease

“…Some reports [37] , but not all [38] , have shown that it can inhibit NF-B activation in renal mesangial and epithelial cells. Interventional animal studies have confirmed the nephroprotective properties of NAC in cyclosporine-and mercury-induced nephrotoxicity as well as in ischemia/ reperfusion injury [39][40][41][42] . The attenuation of histological abnormalities involving tubular injury as well as preservation of renal function were observed after NAC.…”