Unveiling the Role of Selenium in Child Development: Impacts on Growth, Neurodevelopment and Immunity

Abstract

Selenium (Se) is a vital trace element for children, playing a crucial role in numerous physiological processes, including antioxidant defense, immune regulation, thyroid function, and bone metabolism. Emerging evidence highlights its potential impact on child development and growth while also underscoring the complexity of its mechanisms and the global variations in Se intake. The aim of this review is to comprehensively elucidate the significance of Se in various biological processes within the human body, with a focus on its role in child development and growth; its biochemical effects on the nervous system, thyroid function, immune system, and bone tissue; and the implications of Se deficiency and toxicity. This review integrates findings from experimental models, epidemiological studies, and clinical trials to explore Se's role in neurodevelopment, growth regulation, and immune competence in children. Selenoproteins, which regulate oxidative stress and thyroid hormone and bone metabolism, are essential for normal growth and cognitive development in children. Se deficiency and toxicity has been linked to impaired immune function, growth retardation, and decreased immune function. The findings underscore Se's influence on various biological pathways that are critical for healthy child development and its broader importance for child health. Public health strategies aimed at optimizing selenium intake may play a pivotal role in improving pediatric health outcomes worldwide.

Keywords: Se deficiency; Se toxicity; antioxidant defense; bone metabolism; child development and growth; children; immune regulation; neurodevelopment; selenium; selenoproteins; thyroid function.

Figure 1

Selenium (Se) metabolism in the human body [61]. The metabolism of dietary Se, including its absorption, transport, and distribution. Se from food (e.g., selenomethionine and selenocysteine) is absorbed in the intestine, converted to hydrogen selenide (H₂Se), and transported to the liver, where it is used for selenoprotein synthesis, including selenoprotein P. Selenoprotein P facilitates Se transport to target tissues such as the brain, kidneys, and bones, supporting essential biological functions.

Figure 2

The role of selenium (Se) in child development and growth [74]. Se is involved in the regulation of neurotransmitter systems, which are critical for cognitive and neural development. Se protects the thyroid gland by contributing to the synthesis and regulation of thyroid hormones (T3 and T4), reducing the risk of thyroid disorders. Se supports healthy puberty and the development of the reproductive system. This is symbolized by a transition from childhood to adolescence, with representations of reproductive organs and hormonal signaling. Se plays a critical role in antioxidant defense by neutralizing ROS. Cells are depicted as shielded from oxidative damage, highlighting selenium’s contribution to cellular health. Selenium enhances immune responses, protecting against infections and modulating immune cell activity.

Figure 3

Selenium-associated pathways contributing to neural damage [104]. Selenium is transported to neurons via its incorporation into selenoprotein P (SELENOP), which interacts with its receptor, low-density lipoprotein receptor-related protein 8 (LRP8), also referred to as apolipoprotein receptor E2 (ApoER2). This mechanism plays a crucial role in maintaining antioxidant defenses by enabling selenoproteins to mitigate the harmful effects of reactive oxygen species (ROS). Dysfunction in selenium transport pathways can lead to the suppression of protective mechanisms, upregulation of harmful gene expression, and the onset of mitochondrial dysfunction resulting from DNA damage. Such impairments are closely linked to the development of neurological disorders, including cognitive impairment.

Figure 4

The role of selenium (Se) in metabolic pathways of inflammation [166]. The figure illustrates the role of selenium in mitigating oxidative stress at the cellular level through its incorporation into selenoproteins. Se modulates the NFkB signaling pathway, a key regulator of pro-inflammatory cytokine genes. This activation of leukocytes leads to increased cytokine expression.