Effect of hydrogen peroxide on normal and acatalasemic mouse erythrocytes

Noriyoshi Masuoka,Ayumi Zukeran,Kazunori Takemoto,Da-Hong Wang,Kohji Ishihara

doi:10.1016/j.toxrep.2020.02.001

Noriyoshi Masuoka, Ayumi Zukeran + Show 3 more

Open Access

https://doi.org/10.1016/j.toxrep.2020.02.001

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Journal: Toxicology Reports	Publication Date: Jan 1, 2020
Citations: 1	License type: cc-by

Affiliation: Okayama University of Science

Abstract

ObjectivesNormal and acatalasemic mouse erythrocytes were used to clarify the relationship between oxidative damage in H2O2-treated erythrocytes and catalase activity. Design & MethodsGeneration of hydrolysis-resistant erythrocytes and hemolysis were examined. The osmotic fragility test, the negative charges and the number of membrane-flickering erythrocytes among the H2O2-treated erythrocytes were investigated. ResultsSmall amounts of hydrolysis-resistant mouse erythrocytes were generated by treatment with 0.1 mM H2O2, and the amount of acatalasemic erythrocytes was larger than untreated controls. Hemolysis in the acatalasemic erythrocytes was observed 30 min after the addition of the H2O2. A drastic increase in hydrolysis-resistant erythrocytes and a loss of membrane proteins in the acatalasemic erythrocytes were found as a result of the addition of 1 mM H2O2. Hemolysis in normal erythrocytes was observed at 3 mM H2O2. ConclusionsCatalase is a potent H2O2-scavenger even in acatalasemic mouse erythrocytes. It is concluded that the drastic increase of hydrolysis-resistant erythrocytes is induced by a loss of membrane function and is associated with the low catalase activity in these cells.

Highlights

Hydrogen peroxide (H2O2), which is one of the reactive oxygen species (ROS), induces oxidative stress in living organisms and is involved in a variety of signaling pathways [1,2,3,4]
When erythrocytes were treated at 1 mM H2O2, the hydrolysis-resistant acatalasemic erythrocytes dramatically increased to 90.1 %, but the ratio in the normal erythrocytes was 15.0 %
This suggests that endogenous H2O2 and the radicals were removed by cytosolic catalase and other scavenging activities in the erythrocytes

Summary

Introduction

Hydrogen peroxide (H2O2), which is one of the reactive oxygen species (ROS), induces oxidative stress in living organisms and is involved in a variety of signaling pathways [1,2,3,4]. As the H2O2-scavenging activity of glutathione peroxidase and peroxiredoxin 2 in erythrocytes is reportedly low [5,6], it is deduced that the catalase [EC1.11.1.6] that is present in erythrocytes is important in the defense against oxidative stress. The residual catalase activity of acatalasemic erythrocytes in Switzerland and Hungary was found to be higher than in Japan, and there has been no report of Takahara’s disease. The gene frequency of acatalasemia in Japan, Switzerland and Hungary is estimated to be 0.08/1000, 0.05/1000 and 0.04/1000, respectively [11]. In 2000, Goth suggested that acatalasemia patients in Hungary were at a higher risk for and an earlier manifestation of diabetes (10 years) [15]. Animal experiments indicated that low catalase activity in blood is associated with mouse diabetes under oxidative stress conditions [16]. The oxidative stress damaged oxidant-sensitive beta cells in the pancreas and thereby induced diabetes, and the beta cell damage was shown to be ameliorated by antioxidants [17,18,19]

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