SELENOH, also known as selenoprotein H and SELH, is a member of the thioredoxin-like family of selenoproteins. Selenoproteins are involved in various functions, with SELENOH potentially playing roles in redox regulation, antioxidant defense, and gene expression regulation in response to redox status [1,5]. It contains a selenocysteine residue in the conserved CXXU motif, which is crucial for its functionally active conformation [5].

In a Selenoh gene knockout (HKO) mouse model, HKO female mice showed a significant decline in cognition, reduced myelin basic protein expression in hippocampal oligodendrocytes, and disrupted hippocampal lipid metabolism, indicating that SELENOH may mediate low selenium-related cognitive decline through these mechanisms [4]. In human colorectal cancer cells, knockdown of SELENOH decreased cellular differentiation, increased proliferation, migration, and the ability to form colonies or tumor xenografts, suggesting SELENOH is a key regulator for cell cycle progression and prevention of uncontrolled proliferation [3]. In the green alga Chlamydomonas reinhardtii, SELENOH-amiRNA knockdown mutants produced more reactive oxygen species (ROS) and grew slower than the wild-type, suggesting it can reduce chromium toxicity by decreasing ROS levels [2].

In conclusion, SELENOH plays essential roles in cognitive function, cell cycle regulation, and redox-related processes. Studies using gene knockout models in mice and knockdown in cell lines have revealed its significance in cognitive decline, tumorigenesis, and response to metal-induced toxicity, providing insights into potential disease mechanisms and the role of selenium-related biology in these conditions.