Glycerol-Induced Acute Renal Failure Attenuates Subsequent HgCl<sub>2</sub>-Associated Nephrotoxicity: Correlation of Renal Function and Morphology

Backenroth, Rebecca; Schuger, Lucy; Wald, Hanna; Popovtzer, Mordecai M.

doi:10.3109/08860229809045086

Cited by 12 publications

(3 citation statements)

References 19 publications

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“…HO-1 mRNA is also induced in the kidney as early as 3-6 h after injury in ischemia-reperfusion (132,200) and nephrotoxic acute renal failure (1,90,243), models not dependent on filtered heme proteins. Renal tubular induction of HO-1 is protective in these models as well (21,200,201,243). Modulation of HO-1 expression using chemical inducers, inhibitors, and HO-1 gene delivery also support a functional role for HO-1 expression in ischemia-reperfusion injury in the liver (17), brain (163,181), and heart (45,78).…”

Section: Functional Relevance Of Ho-1 Induction In Renal Injurymentioning

confidence: 72%

The story so far: molecular regulation of the heme oxygenase-1 gene in renal injury

Sikorski

Hock

Hill‐Kapturczak

et al. 2004

American Journal of Physiology-Renal Physiology

226

193

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Heme oxygenases (HOs) catalyze the rate-limiting step in heme degradation, resulting in the formation of iron, carbon monoxide, and biliverdin, the latter of which is subsequently converted to bilirubin by biliverdin reductase. Recent attention has focused on the biological effects of product(s) of this enzymatic reaction, which have important antioxidant, anti-inflammatory, and cytoprotective functions. Two major isoforms of the HO enzyme have been described: an inducible isoform, HO-1, and a constitutively expressed isoform, HO-2. A third isoform, HO-3, closely related to HO-2, has also been described. Several stimuli implicated in the pathogenesis of renal injury, such as heme, nitric oxide, growth factors, angiotensin II, cytokines, and nephrotoxins, induce HO-1. Induction of HO-1 occurs as an adaptive and beneficial response to these stimuli, as demonstrated by studies in renal and non-renal disease states. This review will focus on the molecular regulation of the HO-1 gene in renal injury and will highlight the interspecies differences, predominantly between the rodent and human HO-1 genes.

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Section: Functional Relevance Of Ho-1 Induction In Renal Injurymentioning

confidence: 72%

The story so far: molecular regulation of the heme oxygenase-1 gene in renal injury

Sikorski

Hock

Hill‐Kapturczak

et al. 2004

American Journal of Physiology-Renal Physiology

226

193

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“…Our findings of mTAL damage attenuation by prior renal insult may be explained in part by non-specific tubular protection by repeated insults, perhaps mediated by the activation of protective cellular mechanisms, such as heat-shock proteins and heme-oxygenase [27, 28, 29, 30, 31]. Nevertheless, the nephrotoxins utilized as well as the ischemia-reflow insult were primarily directed at the proximal tubule, whereas protection was detected at the distal nephron.…”

Section: Discussionmentioning

confidence: 88%

Proximal Tubular Injury Attenuates Outer Medullary Hypoxic Damage: Studies in Perfused Rat Kidneys

Heyman¹,

Shina²,

Brezis³

et al. 2002

Nephron Exp Nephrol

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The straight segment (S3) of the proximal tubule is predominantly damaged during renal ischemia-reflow, whereas medullary thick ascending limbs (mTALs) are principally affected in other models of hypoxic acute tubular necrosis (ATN). Since the latter injury pattern largely depends on the extent of reabsorptive activity during hypoxic stress, we hypothesized that proximal tubular damage might attenuate downstream mTAL injury by means of diminished distal solute delivery for reabsorption. In isolated rat kidneys perfused for 90 min with oxygenated Krebs-Henseleit solution, mTAL necrosis developed in 75 ± 3% of tubules in the mid-inner stripe of the outer medulla. By contrast, S3 segments in the outer stripe were minimally affected, with tubular fragmentation involving some 5 ± 2% of tubules. In kidneys subjected in vivo to proximal tubular injury and subsequently used for isolated perfusion studies, the injury pattern was inverted: following 20 and 30 min ischemia and reflow for 24 h, S3 fragmentation rose to 18 ± 16% and 72 ± 13%, while mTAL damage was reduced to 33 ± 10 and 24 ± 8%, respectively. In kidneys subjected in vivo to D-serine S3 necrosis rose to 100%, while mTAL damage fell to 1 ± 1% (p < 0.001). Substantial S3 tubular collapse (involving approximately 30% of tubules) and inner stripe interstitial hemorrhage were also noted, exclusively in kidneys subjected to ischemia-reflow. Proximal tubular necrosis alone or in combination with collapse inversely correlated with mTAL necrosis (R = –0.51 and –0.72, respectively, p < 0.003). This cogent inverse association might imply that disruption of the proximal nephron attenuates downstream mTAL necrosis by a reduction of distal tubular reabsorptive workload.

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“…Muscle breakdown products may result in renal failure and even death. 47,48 The LD 50 for glycerol is 0.00442 ml/g. 49…”

Section: Preservationmentioning

confidence: 99%

Guidelines on processing and clinical use of skin allografts

Kearney¹

2005

Clinics in Dermatology

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Processing methods used for banking of skin for subsequent therapeutic use depend on whether the skin is to retain viability or not. For viable skin grafts, sterilisation techniques cannot be applied, however antibiotics and antimycotics may be used to disinfect the tissue with respect to bacteria and fungi. Nevertheless, strict standards are applied to avoid disease transmission from donor to recipient involving donor medical history, donor testing for viral diseases, aseptic retrieval and processing, and control of storage temperature. Cryopreservation is the preferred method for long term storage of viable skin grafts. If viability is not required, then additional long term preservation methods may be used including deep-freezing, freeze-drying or high concentration solute preservation. All three methods work by reducing water activity. In addition it is possible to apply certain sterilisation techniques that have been shown not to damage the tissue. It is important that sterilisation methods are validated in accordance with precise definitions of sterilisation, and for the initial levels of "bioburden" expected to be present immediately prior to application of the sterilisation method. The application of improved and refined methodologies in accordance with defined standards has ensured improved graft performance while reducing risk to the recipient.

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Glycerol-Induced Acute Renal Failure Attenuates Subsequent HgCl₂-Associated Nephrotoxicity: Correlation of Renal Function and Morphology

Cited by 12 publications

References 19 publications

The story so far: molecular regulation of the heme oxygenase-1 gene in renal injury

The story so far: molecular regulation of the heme oxygenase-1 gene in renal injury

Proximal Tubular Injury Attenuates Outer Medullary Hypoxic Damage: Studies in Perfused Rat Kidneys

Guidelines on processing and clinical use of skin allografts

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Glycerol-Induced Acute Renal Failure Attenuates Subsequent HgCl2-Associated Nephrotoxicity: Correlation of Renal Function and Morphology

Cited by 12 publications

References 19 publications

The story so far: molecular regulation of the heme oxygenase-1 gene in renal injury

The story so far: molecular regulation of the heme oxygenase-1 gene in renal injury

Proximal Tubular Injury Attenuates Outer Medullary Hypoxic Damage: Studies in Perfused Rat Kidneys

Guidelines on processing and clinical use of skin allografts

Contact Info

Product

Resources

About

Glycerol-Induced Acute Renal Failure Attenuates Subsequent HgCl₂-Associated Nephrotoxicity: Correlation of Renal Function and Morphology