Abstract
Galactose is a ubiquitous monosaccharide with important yet incompletely understood nutritive and physiological roles. Chronic parenteral d-galactose administration is used for modeling aging-related pathophysiological processes in rodents due to its ability to induce oxidative stress (OS). Conversely, chronic oral d-galactose administration prevents and alleviates cognitive decline in a rat model of sporadic Alzheimer’s disease, indicating that galactose may exert beneficial health effects by acting in the gut. The present aim was to explore the acute time-response of intestinal redox homeostasis following oral administration of d-galactose. Male Wistar rats were euthanized at baseline (n = 6), 30 (n = 6), 60 (n = 6), and 120 (n = 6) minutes following orogastric administration of d-galactose (200 mg/kg). The overall reductive capacity, lipid peroxidation, the concentration of low-molecular-weight thiols (LMWT) and protein sulfhydryls (SH), the activity of Mn and Cu/Zn superoxide dismutases (SOD), reduced and oxidized fractions of nicotinamide adenine dinucleotide phosphates (NADPH/NADP), and the hydrogen peroxide dissociation rate were analyzed in duodenum and ileum. Acute oral administration of d-galactose increased the activity of SODs and decreased intestinal lipid peroxidation and nucleophilic substrates (LMWT, SH, NADPH), indicating activation of peroxidative damage defense pathways. The redox system of the small intestine can acutely tolerate even high luminal concentrations of galactose (0.55 M), and oral galactose treatment is associated with a reduction rather than the increment of the intestinal OS. The ability of oral d-galactose to modulate intestinal OS should be further explored in the context of intestinal barrier maintenance, and beneficial cognitive effects associated with long-term administration of low doses of d-galactose.
Highlights
IntroductionGalactose is an omnipresent epimer of glucose that was first described by Louis
Galactose is an omnipresent epimer of glucose that was first described by LouisPasteur in 1856 following Erdmann’s observation that hydrolysis of the milk sugar lactose yields a substance that is not glucose
The trends over time were in our focus, we decided to report the results based on group/time-point differences as (i) it was permitted by the design, (ii) we had no sensible time-course model that would assume reasonable changes of variables of interest as a function of the exposure time, (iii) we considered that this “conservative”
Summary
Galactose is an omnipresent epimer of glucose that was first described by Louis. Pasteur in 1856 following Erdmann’s observation that hydrolysis of the milk sugar lactose yields a substance that is not glucose. Both in its free form and attached to other molecules forming oligo- or polysaccharides, glycolipids, or glycoproteins, galactose is ubiquitous in all living organisms [1]. Together with glucose (in the form of disaccharide lactose) galactose is a cornerstone of animal milk that provides structural and metabolic support during the most sensitive developmental period [1]. Oxidative stress (OS) has been proposed as the main driver mediating galactose-induced senescence, exact pathophysiological mechanisms mediating
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