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Osaka, Japan – A recent study published in Blood by researchers from Osaka University and other Japanese institutions highlights the critical role of selenoproteins in protecting cells from age-related damage. The findings emphasize how these antioxidant molecules counteract harmful reactive oxygen species (ROS) and support the proper function of hematopoietic stem cells (HSCs), which are essential for blood cell production.
The Role of Selenoproteins in Antioxidant Defense
Many foods are marketed for their antioxidant properties, as antioxidants help neutralize ROS—chemically reactive molecules that can disrupt normal cellular functions. The accumulation of ROS has been linked to various age-related diseases, including cancer. Among the antioxidants in the human body, selenoproteins play a crucial role in converting harmful ROS, such as lipid peroxides, into safer compounds.
Human cells contain 25 different selenoproteins, which act as antioxidant enzymes. The study reveals that lipid peroxidation, caused by ROS buildup, can negatively affect hematopoietic stem cells, leading to aging-related dysfunction.
Investigating the Effects of Selenoprotein Disruption
The research team used a mouse model with a specific gene knocked out, leading to disrupted selenoprotein production. Their findings showed that this disruption particularly affected hematopoietic stem cells and immune cells belonging to the B cell lineage (a type of white blood cell). However, myeloid cells, another type of immune cell, remained largely unaffected.
“The most notable result was B lymphocytopenia, which means there were fewer B cells than expected,” explained Hiromi Yamazaki, co-lead author of the study. “Additionally, HSCs showed a reduced ability to self-renew.”
Further analysis indicated that the observed aging-related effects were driven by lipid peroxidation. Notably, the study found that when selenoprotein synthesis was disrupted, B cell progenitors were more likely to switch to the myeloid cell lineage.
Potential Implications for Aging and Disease Prevention
“Our data suggest clear lineage-specific effects when the protective role of selenoproteins is lost,” said Daichi Inoue, senior author of the study. “These enzymes are critical for counteracting lipid peroxides that accumulate during aging.”
The researchers also conducted feeding experiments on the knockout mice and discovered that dietary vitamin E could protect hematopoiesis and help restore proper B cell differentiation. This finding suggests that addressing selenoprotein-related deficiencies could be a potential strategy for combating age-related diseases.
Future Research and Applications
These results highlight the importance of maintaining a proper oxidant/antioxidant balance in the body. Given that knockout mice displayed similar aging characteristics to normal aged mice, the study underscores the potential for dietary and medical interventions targeting selenoprotein pathways.
Further research may explore whether enhancing selenoprotein activity in humans could serve as a therapeutic approach to mitigate aging-related cellular damage and support immune function.
Disclaimer: This article is for informational purposes only and does not constitute medical advice. Readers should consult healthcare professionals before making any dietary or lifestyle changes based on these findings.
Reference: Yumi Aoyama et al, Selenoprotein-Mediated Redox Regulation Shapes the Cell Fate of HSCs and Mature Lineages, Blood (2025). DOI: 10.1182/blood.2024025402
