Hepatic methanethiol oxidase (MTO) activity of mice requires adequate dietary supply of copper
5 affiliations
- 1Institute of Nutritional Sciences, Nutrigenomics Section, Friedrich Schiller University Jena, Jena, Germany
- 2Institute of Nutritional Sciences, Department of Nutritional Physiology, Friedrich Schiller University Jena, Jena, Germany
- 3Institute of Toxicology and Environmental Hygiene, Technical University Munich, School of Medicine and Health, Munich, Germany; Institute of Molecular Toxicology and Pharmacology, Helmholtz Center Munich, German Research Center for Environmental Health, Neuherberg, Germany
- 4Institute of Nutritional Sciences, Department of Nutritional Physiology, Friedrich Schiller University Jena, Jena, Germany; Corresponding author.
- 5Institute of Nutritional Sciences, Nutrigenomics Section, Friedrich Schiller University Jena, Jena, Germany; Corresponding author. Institute of Nutritional Sciences, Friedrich Schiller University Jena, Dornburger Str. 24-29, D-07743, Jena, Germany.
Abstract
Selenium-binding protein 1 (SELENBP1) catalyzes the oxidative conversion of methanethiol to hydrogen sulfide, hydrogen peroxide and formaldehyde. Methanethiol oxidase (MTO) activity of recombinant human SELENBP1 was shown to require copper (Cu) ions, whereas selenium (Se) was largely dispensable. However, the impact of Cu and Se on MTO activity in mammals has not been explored so far. To investigate whether SELENBP1 levels and MTO activity in mice are affected by dietary availability of trace elements, liver samples of C57BL/6JRj mice held on diets deficient in Cu and/or Se for eight weeks were analyzed, as compared to mice fed the control diet with adequate trace element supply. Dietary Cu deficiency always resulted in diminished hepatic MTO activity, as detected by methanethiol-derived production of hydrogen sulfide. The effect of Cu deficiency was more pronounced in male than in female mice. Se deficiency only slightly, and solely in males, lowered MTO activity. Another sex-specific effect was observed with hepatic SELENBP1 levels: whereas diets deficient in Cu and/or Se increased SELENBP1 levels in males, they were decreased in female mice under Cu-deficient conditions. In addition to dietary Cu deficiency, MTO activity and SELENBP1 levels were explored in a rat model of Wilson's disease, which is characterized by hepatic Cu accumulation. Hepatic MTO activity was not altered in male and female rats under conditions of excess intrahepatic Cu, as long as the liver was not severely damaged. Notwithstanding the relatively low number of 5-6 animals included in each group, our data allow for the conclusion that hepatic MTO activity depends on adequate dietary Cu supply, whereas excess Cu does not further enhance the MTO activity of SELENBP1.
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BibTeX
@article{krafczyk2026hepatic,
title = {{Hepatic methanethiol oxidase (MTO) activity of mice requires adequate dietary supply of copper}},
author = {Niklas Krafczyk and Kristina Lossow and Lara Biegel and Nora Meinhardt and Maria Schwarz and Hans Zischka and Holger Steinbrenner and Anna Patricia Kipp and Lars-Oliver Klotz},
journal = {Redox Biology},
year = {2026},
month = oct,
doi = {10.1016/j.redox.2026.104384},
url = {https://doi.org/10.1016/j.redox.2026.104384},
note = {CC BY},
}
RIS
TY - JOUR
TI - Hepatic methanethiol oxidase (MTO) activity of mice requires adequate dietary supply of copper
AU - Niklas Krafczyk
AU - Kristina Lossow
AU - Lara Biegel
AU - Nora Meinhardt
AU - Maria Schwarz
AU - Hans Zischka
AU - Holger Steinbrenner
AU - Anna Patricia Kipp
AU - Lars-Oliver Klotz
PY - 2026
DA - 2026/10/30
JO - Redox Biology
DO - 10.1016/j.redox.2026.104384
UR - https://doi.org/10.1016/j.redox.2026.104384
AB - Selenium-binding protein 1 (SELENBP1) catalyzes the oxidative conversion of methanethiol to hydrogen sulfide, hydrogen peroxide and formaldehyde. Methanethiol oxidase (MTO) activity of recombinant human SELENBP1 was shown to require copper (Cu) ions, whereas selenium (Se) was largely dispensable. However, the impact of Cu and Se on MTO activity in mammals has not been explored so far. To investigate whether SELENBP1 levels and MTO activity in mice are affected by dietary availability of trace elements, liver samples of C57BL/6JRj mice held on diets deficient in Cu and/or Se for eight weeks were analyzed, as compared to mice fed the control diet with adequate trace element supply. Dietary Cu deficiency always resulted in diminished hepatic MTO activity, as detected by methanethiol-derived production of hydrogen sulfide. The effect of Cu deficiency was more pronounced in male than in female mice. Se deficiency only slightly, and solely in males, lowered MTO activity. Another sex-specific effect was observed with hepatic SELENBP1 levels: whereas diets deficient in Cu and/or Se increased SELENBP1 levels in males, they were decreased in female mice under Cu-deficient conditions. In addition to dietary Cu deficiency, MTO activity and SELENBP1 levels were explored in a rat model of Wilson's disease, which is characterized by hepatic Cu accumulation. Hepatic MTO activity was not altered in male and female rats under conditions of excess intrahepatic Cu, as long as the liver was not severely damaged. Notwithstanding the relatively low number of 5-6 animals included in each group, our data allow for the conclusion that hepatic MTO activity depends on adequate dietary Cu supply, whereas excess Cu does not further enhance the MTO activity of SELENBP1.
SN - 2213-2317
ER -