Publication

Inadequate Antioxidative Responses in Kidneys of Brain-Dead Rats

Hoeksma, D., Rebolledo, R. A., Hottenrott, M., Bodar, Y. S., Wiersema-Buist, J. J., Van Goor, H. & Leuvenink, H. G. D., Apr-2017, In : Transplantation. 101, 4, p. 746-753 8 p.

Research output: Contribution to journalArticleAcademicpeer-review

APA

Hoeksma, D., Rebolledo, R. A., Hottenrott, M., Bodar, Y. S., Wiersema-Buist, J. J., Van Goor, H., & Leuvenink, H. G. D. (2017). Inadequate Antioxidative Responses in Kidneys of Brain-Dead Rats. Transplantation, 101(4), 746-753. https://doi.org/10.1097/TP.0000000000001417

Author

Hoeksma, Dane ; Rebolledo, Rolando A. ; Hottenrott, Maximilia ; Bodar, Yves S. ; Wiersema-Buist, Janneke J. ; Van Goor, Harry ; Leuvenink, Henri G. D. / Inadequate Antioxidative Responses in Kidneys of Brain-Dead Rats. In: Transplantation. 2017 ; Vol. 101, No. 4. pp. 746-753.

Harvard

Hoeksma, D, Rebolledo, RA, Hottenrott, M, Bodar, YS, Wiersema-Buist, JJ, Van Goor, H & Leuvenink, HGD 2017, 'Inadequate Antioxidative Responses in Kidneys of Brain-Dead Rats', Transplantation, vol. 101, no. 4, pp. 746-753. https://doi.org/10.1097/TP.0000000000001417

Standard

Inadequate Antioxidative Responses in Kidneys of Brain-Dead Rats. / Hoeksma, Dane; Rebolledo, Rolando A.; Hottenrott, Maximilia; Bodar, Yves S.; Wiersema-Buist, Janneke J.; Van Goor, Harry; Leuvenink, Henri G. D.

In: Transplantation, Vol. 101, No. 4, 04.2017, p. 746-753.

Research output: Contribution to journalArticleAcademicpeer-review

Vancouver

Hoeksma D, Rebolledo RA, Hottenrott M, Bodar YS, Wiersema-Buist JJ, Van Goor H et al. Inadequate Antioxidative Responses in Kidneys of Brain-Dead Rats. Transplantation. 2017 Apr;101(4):746-753. https://doi.org/10.1097/TP.0000000000001417


BibTeX

@article{41f8a4ad4e5246c79a6bb66d62fc7a52,
title = "Inadequate Antioxidative Responses in Kidneys of Brain-Dead Rats",
abstract = "Background. Brain death (BD)-related lipid peroxidation, measured as serum malondialdehyde (MDA) levels, correlates with delayed graft function in renal transplant recipients. How BD affects lipid peroxidation is not known. The extent of BD-induced organ damage is influenced by the speed at which intracranial pressure increases. To determine possible underlying causes of lipid peroxidation, we investigated the renal redox balance by assessing oxidative and antioxidative processes in kidneys of brain-dead rats after fast and slow BD induction. Methods. Brain death was induced in 64 ventilated male Fisher rats by inflating a 4.0F Fogarty catheter in the epidural space. Fast and slow inductions were achieved by an inflation speed of 0.45 and 0.015 mL/min, respectively, until BD confirmation. Healthy non-brain-dead rats served as reference values. Brain-dead rats were monitored for 0.5, 1, 2, or 4 hours, after which organs and blood were collected. Results. Increased MDA levels became evident at 2 hours of slow BD induction at which increased superoxide levels, decreased glutathione peroxidase (GPx) activity, decreased glutathione levels, increased inducible nitric oxide synthase and heme-oxygenase 1 expression, and increased plasma creatinine levels were evident. At 4 hours after slow BD induction, superoxide, MDA, and plasma creatinine levels increased further, whereas GPx activity remained decreased. Increased MDA and plasma creatinine levels also became evident after 4 hours fast BD induction. Conclusion. Brain death leads to increased superoxide production, decreased GPx activity, decreased glutathione levels, increased inducible nitric oxide synthase and heme-oxygenase 1 expression, and increased MDA and plasma creatinine levels. These effects were more pronounced after slow BD induction. Modulation of these processes could lead to decreased incidence of delayed graft function.",
keywords = "ACUTE-RENAL-FAILURE, DELAYED GRAFT FUNCTION, NITRIC-OXIDE SYNTHASE, OXIDATIVE STRESS, HEME OXYGENASE-1, FREE-RADICALS, GLUTATHIONE-PEROXIDASE, LIPID-PEROXIDATION, SUBARACHNOID HEMORRHAGE, SUPEROXIDE-DISMUTASE",
author = "Dane Hoeksma and Rebolledo, {Rolando A.} and Maximilia Hottenrott and Bodar, {Yves S.} and Wiersema-Buist, {Janneke J.} and {Van Goor}, Harry and Leuvenink, {Henri G. D.}",
year = "2017",
month = "4",
doi = "10.1097/TP.0000000000001417",
language = "English",
volume = "101",
pages = "746--753",
journal = "Transplantation",
issn = "0041-1337",
publisher = "LIPPINCOTT WILLIAMS & WILKINS",
number = "4",

}

RIS

TY - JOUR

T1 - Inadequate Antioxidative Responses in Kidneys of Brain-Dead Rats

AU - Hoeksma, Dane

AU - Rebolledo, Rolando A.

AU - Hottenrott, Maximilia

AU - Bodar, Yves S.

AU - Wiersema-Buist, Janneke J.

AU - Van Goor, Harry

AU - Leuvenink, Henri G. D.

PY - 2017/4

Y1 - 2017/4

N2 - Background. Brain death (BD)-related lipid peroxidation, measured as serum malondialdehyde (MDA) levels, correlates with delayed graft function in renal transplant recipients. How BD affects lipid peroxidation is not known. The extent of BD-induced organ damage is influenced by the speed at which intracranial pressure increases. To determine possible underlying causes of lipid peroxidation, we investigated the renal redox balance by assessing oxidative and antioxidative processes in kidneys of brain-dead rats after fast and slow BD induction. Methods. Brain death was induced in 64 ventilated male Fisher rats by inflating a 4.0F Fogarty catheter in the epidural space. Fast and slow inductions were achieved by an inflation speed of 0.45 and 0.015 mL/min, respectively, until BD confirmation. Healthy non-brain-dead rats served as reference values. Brain-dead rats were monitored for 0.5, 1, 2, or 4 hours, after which organs and blood were collected. Results. Increased MDA levels became evident at 2 hours of slow BD induction at which increased superoxide levels, decreased glutathione peroxidase (GPx) activity, decreased glutathione levels, increased inducible nitric oxide synthase and heme-oxygenase 1 expression, and increased plasma creatinine levels were evident. At 4 hours after slow BD induction, superoxide, MDA, and plasma creatinine levels increased further, whereas GPx activity remained decreased. Increased MDA and plasma creatinine levels also became evident after 4 hours fast BD induction. Conclusion. Brain death leads to increased superoxide production, decreased GPx activity, decreased glutathione levels, increased inducible nitric oxide synthase and heme-oxygenase 1 expression, and increased MDA and plasma creatinine levels. These effects were more pronounced after slow BD induction. Modulation of these processes could lead to decreased incidence of delayed graft function.

AB - Background. Brain death (BD)-related lipid peroxidation, measured as serum malondialdehyde (MDA) levels, correlates with delayed graft function in renal transplant recipients. How BD affects lipid peroxidation is not known. The extent of BD-induced organ damage is influenced by the speed at which intracranial pressure increases. To determine possible underlying causes of lipid peroxidation, we investigated the renal redox balance by assessing oxidative and antioxidative processes in kidneys of brain-dead rats after fast and slow BD induction. Methods. Brain death was induced in 64 ventilated male Fisher rats by inflating a 4.0F Fogarty catheter in the epidural space. Fast and slow inductions were achieved by an inflation speed of 0.45 and 0.015 mL/min, respectively, until BD confirmation. Healthy non-brain-dead rats served as reference values. Brain-dead rats were monitored for 0.5, 1, 2, or 4 hours, after which organs and blood were collected. Results. Increased MDA levels became evident at 2 hours of slow BD induction at which increased superoxide levels, decreased glutathione peroxidase (GPx) activity, decreased glutathione levels, increased inducible nitric oxide synthase and heme-oxygenase 1 expression, and increased plasma creatinine levels were evident. At 4 hours after slow BD induction, superoxide, MDA, and plasma creatinine levels increased further, whereas GPx activity remained decreased. Increased MDA and plasma creatinine levels also became evident after 4 hours fast BD induction. Conclusion. Brain death leads to increased superoxide production, decreased GPx activity, decreased glutathione levels, increased inducible nitric oxide synthase and heme-oxygenase 1 expression, and increased MDA and plasma creatinine levels. These effects were more pronounced after slow BD induction. Modulation of these processes could lead to decreased incidence of delayed graft function.

KW - ACUTE-RENAL-FAILURE

KW - DELAYED GRAFT FUNCTION

KW - NITRIC-OXIDE SYNTHASE

KW - OXIDATIVE STRESS

KW - HEME OXYGENASE-1

KW - FREE-RADICALS

KW - GLUTATHIONE-PEROXIDASE

KW - LIPID-PEROXIDATION

KW - SUBARACHNOID HEMORRHAGE

KW - SUPEROXIDE-DISMUTASE

U2 - 10.1097/TP.0000000000001417

DO - 10.1097/TP.0000000000001417

M3 - Article

C2 - 27495771

VL - 101

SP - 746

EP - 753

JO - Transplantation

JF - Transplantation

SN - 0041-1337

IS - 4

ER -

ID: 35240212