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Selenomethionine administration decreases the oxidative stress induced by post mortem ischemia in the heart, liver and kidneys of rats

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Abstract

Selenium is an essential element in human and animal metabolism integrated into the catalytic site of glutathione peroxidase (GPX1), an antioxidant enzyme that protects cells from damage caused by reactive oxygen species (ROS). Oxidative stress refers the imbalance between ROS and antioxidant defense systems. It generates alterations of DNA, proteins and lipid peroxidation. The imbalance occurs particularly during ischemia and lack of postmortem perfusion. This mechanism is of relevance in transplant organs, affecting their survival. The aim of this research is to evaluate the effect of seleno-methionine (SeMet) as a protective agent against postmortem ischemia injury in transplant organs. Wistar rats were orally administered with SeMet. After sacrifice, liver, heart and kidney samples were collected at different postmortem intervals (PMIs). SeMet administration produced a significant increase of Se concentration in the liver (65%, p < 0.001), heart (40%, p < 0.01) and kidneys (45%, p < 0.05). Levels of the oxidative stress marker malondialdehyde (MDA) decreased significantly compared to control in the heart (0.21 ± 0.04 vs. 0.12 ± 0.02 mmol g−1) and kidneys (0.41 ± 0.02 vs. 0.24 ± 0.03 mmol g−1) in a PMI of 1–12 h (p < 0.01). After SeMet administration for 21 days, a significant increase in GPX1 activity was observed in the liver (80%, p < 0.001), kidneys (74%, p < 0.01) and heart (35%, p < 0.05). SeMet administration to rats significantly decreased the oxidative stress in the heart, liver and kidneys of rats generated by postmortem ischemia.

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Additional/raw data can be made available upon request.

Abbreviations

SeMet:

Selenomethionine

GPX1:

Glutathione peroxidase 1

SeCys:

Selenocysteine

ROS:

Reactive oxygen species

MDA:

Malondialdehyde

TBA:

2-Thiobarbituric acid

LC:

Liquid chromatography

ICP MS:

Inductively coupled plasma mass spectrometry

PMI:

Postmortem interval

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Acknowledgements

The authors wish to acknowledge the financial support received by the Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET), Agencia Nacional de Promoción Científica y Técnica (ANPCyT) and the Universidad Nacional de San Luis (UNSL).

Funding

This work was supported by the Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET) [1 Grant, Hasuoka], the Agencia Nacional de Promoción Científica y Técnica (ANPCyT) and the Universidad Nacional de San Luis (UNSL).

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Authors and Affiliations

  1. Instituto de Química San Luis (INQUISAL-CONICET), Chacabuco y Pedernera, 5700, San Luis, Argentina

    Paul E. Hasuoka & Pablo H. Pacheco

  2. Facultad de Química, Bioquímica y Farmacia, Universidad Nacional de San Luis, Chacabuco y Pedernera, 5700, San Luis, Argentina

    Juan P. Iglesias, Mauricio Teves, Marcos M. Kaplan & Nelson H. Ferrúa

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  1. Paul E. Hasuoka
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  2. Juan P. Iglesias
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  3. Mauricio Teves
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  4. Marcos M. Kaplan
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  5. Nelson H. Ferrúa
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  6. Pablo H. Pacheco
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Correspondence to Pablo H. Pacheco.

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All animal experimentation was reviewed and approved by the Animal Care and Use Institutional Committee of the Universidad Nacional de San Luis (Ord. 006-02, Protocol N ° F-293/18 UNSL).

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Hasuoka, P.E., Iglesias, J.P., Teves, M. et al. Selenomethionine administration decreases the oxidative stress induced by post mortem ischemia in the heart, liver and kidneys of rats. Biometals 34, 831–840 (2021). https://doi.org/10.1007/s10534-021-00310-3

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  • DOI: https://doi.org/10.1007/s10534-021-00310-3

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