D-Galactose is utilized in creating animal models, specifically to establish subacute aging models in mice and cataract models in rats. Chronic exposure to D-galactose leads to neurodegeneration characterized by increased caspase-mediated apoptosis and reduced neurogenesis and neuron migration in mice. This exposure also heightens oxidative damage. Consequently, the D-galactose-induced toxicity model in mice serves as an effective tool for exploring the mechanisms underlying neurodegeneration and for evaluating neuroprotective drugs and agents^[2].

Oral administration of D-galactose in rats leads to cognitive impairments, observed as behavioral changes in open-field tests during the 4th and 6th weeks following administration, and as spatial memory deficits in the radial maze test after the 6th week. These cognitive impairments are associated with oxidative damage^[3].

D-Galactose serves as a classical agent for modeling subacute aging and cataracts. It alters the structure of proteins and peptides by reacting with their free amine groups, leading to the non-enzymatic glycation and subsequent accumulation of advanced glycation end products (AGEs). These AGEs contribute to age-related disorders. Rats and mice are commonly employed as animal models in this context^[4][5][6][7].

Galactose plays a crucial role in the survival and virulence of bacteria. In Escherichia coli, galactose is metabolized via the Leloir pathway. The two anomers of D-galactose serve distinct functions: α-D-galactose is utilized as a carbon source, while β-D-galactose induces the synthesis of UDP-galactose, which is essential for biosynthetic glycosylation^[1].