The effect of acute oral galactose administration on the redox system of the rat small intestine

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 galactose may exert beneficial health effects by acting in the gut. The present aim was to explore 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 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.

The absence of gastrointestinal redox dyshomeostasis in the brain-first rat model of Parkinson’s disease induced by bilateral intrastriatal 6-hydroxydopamine

“…The latter is further supported by the fact that the same biomarkers have been shown to be sufficiently sensitive to detect redox-related alterations induced by relatively mild stimuli (e.g. single orogastric administration of the 200 mg/kg D-galactose solution)[37] and in other neurotoxin-based models of brain-first-induced neurodegeneration [31, 32].…”

“…Low molecular weight thiols (with glutathione (GSH) being the most abundant) and free protein sulfhydryls (SH) were quantified by measuring 5-thio-2-nitrobenzoic acid (TNB) following the reaction of 5,5⍰-dithio-bis(2-nitrobenzoic acid) (DTNB) with the supernatant and the pellet after precipitation of proteins with sulfosalicylic acid [31, 36, 37]. Briefly, 25 μL of each homogenate was incubated with 4% w/v sulfosalicylic acid in ddH 2 O for 1 h on ice in a 1:1 volumetric ratio.…”

“…The activity of superoxide dismutase (SOD) was determined indirectly by the inhibition of the 1,2,3-trihydroxybenzene (THB) autoxidation [38, 39] using a modified protocol [37, 40]. The homogenates (3 μl for duodenum or 6 μl for ileum and colon) were placed in a 96-well plate and incubated with a 100 μl of the buffer for measuring total SOD activity (80 μL of the THB solution (60 mM THB dissolved in 1 mM HCl) added to 4000 μL of 0.05 M Tris-HCl and 1 mM Na2EDTA (pH 8.2)) or Fe/Mn-SOD activity ((80 μL of the THB solution (60 mM THB dissolved in 1 mM HCl) added to 4000 μL of 0.05 M Tris-HCl, 1 mM Na2EDTA, 2 mM KCN (pH 8.2)).…”

Continued exposure to D‐galactose in postnatal period may inhibit excessive primordial follicle reduction in rats exposed prenatally to D‐galactose

“…A subtle point that should be considered in this study is switching the D‐galactose intake way from the mother's bloodstream during fetal life to the gastrointestinal tract during the infancy period by lactation. Recently, Homolka et al (2022) have shown that the small intestinal redox system is activated under high amounts of oral D‐galactose, creating a protective barrier against oxidative stress and protecting cells from oxidative damage. Oxygen metabolism produces superoxide (SO), which causes many types of cell damage.…”

In vitro analysis of catalase and superoxide dismutase mimetic properties of blue tattoo ink

“…Catalase-like activity CAT solution was prepared by dissolving 1 mg of lyophilized bovine liver CAT powder (Sigma Aldrich, USA) in 10 ml of phosphate-buffered saline (PBS) (pH 7.4). CAT activity was measured using the method first described by Hadwan [18] and adapted in [19]. Briefly, the samples were incubated with 50 μl of the substrate solution (2-10 mM H2O2 in PBS) and the reaction was stopped by adding 150 μl of the Co(NO3)2 stop solution (5 mL Co(NO3)2 x 6 H2O (0.2 g in 10 mL ddH2O) + 5 mL (NaPO3)6 (0.1 g in 10 mL ddH2O) added to 90 mL of NaHCO3 (9 g in 100 mL ddH2O)).…”