Galactose is a simple sugar, a monosaccharide, which is a key component of various biological processes. It is commonly used in cosmetic and pharmaceutical formulations for its hydrating and skin-conditioning properties.

Chemical Composition and Structure

Galactose is a hexose sugar, meaning it contains six carbon atoms. It is an isomer of glucose and has the chemical formula C₆H₁₂O₆. The structure of galactose features a six-membered ring with five carbons and one oxygen, forming a pyranose ring. It has hydroxyl groups (-OH) attached to each carbon, which contribute to its reactivity and solubility.

Physical Properties

Galactose appears as a white, crystalline powder. It is highly soluble in water and has a sweet taste, although less sweet than glucose. The solubility and low sweetness make it suitable for various cosmetic and pharmaceutical formulations. It is stable under normal storage conditions and does not cause significant irritation when applied to the skin.

Production Process 

Galactose is produced through several methods, including:

• Hydrolysis of Lactose: Galactose can be obtained from lactose, a disaccharide found in milk, through hydrolysis. This process involves the enzymatic breakdown of lactose using lactase enzyme, which separates it into glucose and galactose.
• Chemical Synthesis: Galactose can also be synthesized chemically through processes involving complex reactions and the use of different chemical reagents. However, this method is less common compared to enzymatic hydrolysis.
• Purification: The galactose obtained from these processes is purified to remove any impurities and by-products. Purification typically involves crystallization, filtration, and other techniques to ensure a high-purity product.
• Formulation: The purified galactose is incorporated into various formulations. It may be combined with other ingredients to create cosmetic creams, lotions, serums, and pharmaceutical products.
• Quality Control: The final product undergoes rigorous quality control testing to ensure it meets safety, efficacy, and performance standards. This includes checks for purity, stability, and compatibility with other ingredients.
• Storage: Galactose is stored in airtight containers, protected from light, moisture, and heat, to maintain its stability and effectiveness.

Applications 

Medical Galactose is used in pharmaceutical formulations for its role in various metabolic processes (1). It may be used in treatments for certain metabolic disorders and as a component in certain drug formulations (2).

Cosmetics In cosmetic formulations, galactose is valued for its hydrating and skin-conditioning properties. It is used in creams, lotions, and serums to improve skin moisture levels, enhance texture, and support overall skin health.

Others Galactose is also utilized in other applications, including dietary supplements and food products, due to its nutritional benefits and functional properties.

Cosmetics - INCI Functions

• Skin conditioning agent. It is the mainstay of topical skin treatment as it has the function of restoring, increasing or improving skin tolerance to external factors, including melanocyte tolerance. The most important function of the conditioning agent is to prevent skin dehydration, but the subject is rather complex and involves emollients and humectants that can be added in the formulation.

Environmental and Safety Considerations

Galactose is generally considered safe for use in cosmetics and pharmaceuticals when used according to recommended guidelines. It is a naturally occurring sugar with a low risk of irritation or allergic reactions. From an environmental perspective, the production of galactose, especially from natural sources like lactose, is relatively sustainable. However, it is essential to ensure that production processes adhere to sustainable practices to minimize any potential ecological impact.

Molecular Formula  C₆H₁₂O₆

Molecular Weight  

CAS     59-23-4

UNII    X2RN3Q8DNE

EC Number  200-416-4

Synonyms:

D-Galactopyranoside

D-Galactose

D-Gal

D-Galactopyranose

References__________________________________________________________________________

(1) Coelho AI, Berry GT, Rubio-Gozalbo ME. Galactose metabolism and health. Curr Opin Clin Nutr Metab Care. 2015 Jul;18(4):422-7. doi: 10.1097/MCO.0000000000000189. PMID: 26001656.

Abstract. Purpose of review: Galactose - a key source of energy and a crucial structural element in complex molecules - is particularly important for early human development. However, galactose metabolism might be important not only for fetal and neonatal development but also for adulthood, as evidenced by the inherited disorders of galactose metabolism. The purpose of this review is to summarize the current evidence of galactose metabolism in health and disease. Recent findings: The biological importance of galactose goes beyond its importance as a nutrient and a metabolite. Galactose has been selected by evolutionary pressure to exert also a crucial structural role in macromolecules. Additionally, galactose has recently been reported as beneficial in a number of diseases, particularly in those affecting the brain. Summary: Galactose is crucial for human metabolism, with an established role in energy delivery and galactosylation of complex molecules, and evidence for other roles is emerging.

(2) Savin VJ, McCarthy ET, Sharma R, Charba D, Sharma M. Galactose binds to focal segmental glomerulosclerosis permeability factor and inhibits its activity. Transl Res. 2008 Jun;151(6):288-92. doi: 10.1016/j.trsl.2008.04.001.

Abstract. Focal segmental glomerulosclerosis (FSGS) is associated with circulating permeability activity (Palb) and recurs after transplantation in about 30% of patients. The FS permeability factor (FSPF) consists of anionic low-molecular-weight protein(s) that might be excluded by the anionic filtration barrier. We postulated that FSPF may interact with sugars of the glycocalyx, and we tested its affinity for sugars using column chromatography. FSPF showed high affinity for galactose; Palb activity was absent from unbound material and present in eluate after dialysis to remove galactose. In parallel studies, Palb activity of serum was lost after adding galactose > or = 10(-12) M. To determine whether galactose also abolishes plasma Palb activity in vivo, a patient with posttransplant FSGS was given galactose and serum samples were collected. Intravenous infusion of galactose decreased Palb from 0.88 before infusion to undetectable levels postinfusion and at 48 hours. Oral galactose diminished Palb activity; Palb reached a nadir after 2 weeks and remained low for at least 4 weeks after galactose was discontinued. We conclude that FSPF has high affinity for galactose based on chromatography. Additionally, galactose inactivates FSPF and may lead to its clearance from plasma. The interaction between FSPF and glomeruli may depend on FSPF binding to galactose, and the FSPF-galactose complex may be susceptible to uptake by galactose-binding proteins and to catabolism. We propose testing galactose as a novel nontoxic therapy for nephrotic syndrome in FSGS to determine whether galactose slows progression and whether pretransplant therapy decreases rates of recurrence and graft loss.

Paigen K. Role of the galactose pathway in the regulation of beta-galactosidase. J Bacteriol. 1966 Nov;92(5):1394-403. doi: 10.1128/jb.92.5.1394-1403.1966. 

Abstract. Paigen, Kenneth (Roswell Park Memorial Institute, Buffalo, N.Y.). Role of the galactose pathway in the regulation of beta-galactosidase. J. Bacteriol. 92:1394-1403. 1966.-Galactose and its metabolites, galactose-1-phosphate, uridine diphosphogalactose, and uridine diphosphoglucose, as well as metabolites derived from uridine diphosphoglucose, were tested for their role in the regulation of beta-galactosidase. In cultures of wild-type Escherichia coli strains K-12 and B, exogenous galactose was no more effective as a repressor than were other carbon sources. Exogenous galactose also did not repress beta-galactosidase when added to mutants which can accumulate intracellular galactose or galactose-1-phosphate, indicating that these compounds do not repress. In such strains, repression of beta-galactosidase formation did occur if galactose was added in the presence of another metabolizable carbon source. This repression is presumably a consequence of the growth inhibition which follows the accumulation of these compounds, and the general catabolite repression which develops during growth inhibition. Exogenous galactose did repress beta-galactosidase in a mutant which accumulates uridine diphosphogalactose. This appears to result from a combination of several factors. These include a general inhibition of protein synthesis through depletion of the uridine triphosphate pool, catabolite inhibition as a consequence of growth inhibition, as well as a specific inhibition of beta-galactosidase formation. Glucose repression of beta-galactosidase was normal in a mutant strain blocked in the formation of uridine diphosphoglucose from uridine triphosphate and glucose-1-phosphate, indicating that neither uridine diphosphoglucose nor any compound uniquely derived from it functions as the hypothetical catabolite repressor. It is concluded that at least two separate mechanisms exist for the endogenous repression of beta-galactosidase in E. coli. One is exerted by uridine diphosphogalactose or its metabolic product; the other, by the generalized catabolite repressor which is still formed in strains unable to make uridine diphosphogalactose or uridine diphosphoglucose.

Cooper GS, Hulka BS, Baird DD, Savitz DA, Hughes CL Jr, Weinberg CR, Coleman RA, Shields JM. Galactose consumption, metabolism, and follicle-stimulating hormone concentrations in women of late reproductive age. Fertil Steril. 1994 Dec;62(6):1168-75. PMID: 7957979.

Abstract. Objective: To test the hypothesis that high galactose consumption and low activity of galactose-1-phosphate uridyl transferase (transferase) is associated with early ovarian senescence among nongalactosemic women. Design: Cross-sectional study. Data collection consisted of a self-administered questionnaire with sections on diet (food frequency data to measure galactose consumption), reproductive, and medical histories. One blood sample was collected to measure FSH and transferase activity; FSH was used as a measure of ovarian senescence. Among women who were having menstrual periods at least every 8 weeks, the blood sample was drawn in the early follicular phase (days 2 to 4) of a menstrual cycle....Conclusion: These data do not support the hypothesis that low transferase activity represents a genetic predisposition for early ovarian senescence, as measured by FSH levels in women ages 38 to 49 years. However, the hypothesized positive association between galactose consumption and FSH was supported.