B Vitamins, Glucoronolactone and the Immune System: Bioavailability, Doses and Efficiency

Abstract

The present review deals with two main ingredients of energy/power drinks: B vitamins and glucuronolactone and their possible effect on the immune system. There is a strong relationship between the recommended daily dose of selected B vitamins and a functional immune system. Regarding specific B vitamins: (1) Riboflavin is necessary for the optimization of reactive oxygen species (ROS) in the fight against bacterial infections caused by Staphylococcus aureus and Listeria monocytogenes. (2) Niacin administered within normal doses to obese rats can change the phenotype of skeletal fibers, and thereby affect muscle metabolism. This metabolic phenotype induced by niacin treatment is also confirmed by stimulation of the expression of genes involved in the metabolism of free fatty acids (FFAs) and oxidative phosphorylation at this level. (3) Vitamin B5 effects depend primarily on the dose, thus large doses can cause diarrhea or functional disorders of the digestive tract whereas normal levels are effective in wound healing, liver detoxification, and joint health support. (4) High vitamin B6 concentrations (>2000 mg per day) have been shown to exert a significant negative impact on the dorsal root ganglia. Whereas, at doses of approximately 70 ng/mL, sensory symptoms were reported in 80% of cases. (5) Chronic increases in vitamin B12 have been associated with the increased incidence of solid cancers. Additionally, glucuronolactone, whose effects are not well known, represents a controversial compound. (6) Supplementing with D-glucarates, such as glucuronolactone, may help the body's natural defense system function better to inhibit different tumor promoters and carcinogens and their consequences. Cumulatively, the present review aims to evaluate the relationship between the selected B vitamins group, glucuronolactone, and the immune system and their associations to bioavailability, doses, and efficiency.

Keywords: B vitamins; bioavailability; cobalamin; glucuronolactone; immune system; niacin; riboflavin.

Figure 1

The absorption of B vitamins, VB2, vitamin B2 (Riboflavin); VB3, vitamin B3 (Niacin); VB5, vitamin B5 (Pantothenic acid), VB6, vitamin B6 (Pyridoxine); VB12, vitamin B12 (Cobalamin) along the gastrointestinal tract. There are two sources of B vitamins: diet and gut microbiota. As seen, the absorption of vitamins VB2, VB3, VB5, and VB12 from the diet takes place in the small intestine, more precisely in the jejunum. Regarding VB6, the absorption is done at the level of the ileum. In addition, in the ascending colon, there are bacteria that synthesize vitamins VB2, VB3, VB5, and VB6, while VB12 is produced by different bacteria in the descending colon.

Figure 2

Niacin overdose effects. The most well-known side effects include harm to several organs, hypotension, and hepatotoxicity. The morphological alteration of the islets of Langerhans as a result of the impairment and decrease in β pancreatic cell mass was determined after niacin was administered for six weeks. The possible reason for this reduction in β cell mass could be because niacin increases the lipotoxicity of these cells.

Figure 3

VB5 (Panthotenic acid) side effects or VB5 interferences; It is currently unclear how supplemental VB5 interacts with such an extensive variety of medicines. The combination of their administration can be defined by drug hypersensitivity or allergy. Furthermore, VB5 ingestion has been linked to cognitive impairments, according to a medical report.

Figure 4

B vitamins in one carbon metabolism. The enzyme dihydrofolate reductase (DHFR) first converts dietary folate (B9) into dihydrofolate (DHF), which is subsequently reduced to tetrahydrofolate (THF). This process starts the folate cycle. Next, serine hydroxymethyltransferase (SHMT) converts THF to 5,10-methylene THF. This reaction needs B6 as a cofactor and is linked to the hydroxylation of serine (Ser) to glycine (Gly). Deoxyuridine monophosphate (dUMP) is methylated by thymidylate synthase (TS) using 5,10-methylene THF as a methyl donor, resulting in deoxythymidine monophosphate (dTMP). DHF is renewed in this phase to enable further cycling. Alternatively, methylenetetrahydrofolate reductase (MTHFR) can use B2 as a cofactor to decrease 5,10-methylene THF to 5-methytetrahydrofolate (5-mTHF). Methionine synthase (MS) is responsible for catalyzing the methionine cycle, in which 5-mTHF provides a methyl group to regenerate methionine from homocysteine (Hcy). Methionine synthase (MS) needs B12 in the form of methylcobalamin as a cofactor. Methionine adenosyltransferase 2A converts an adenosine to methionine, resulting in the methyl donor S-adenosylmethionine (SAM), which is then used by several methyltransferases (MTs) specific for methylation events involving RNA (RMT), DNA (DNMT), histones (HMT), and proteins (PRMT). S-adenosylhomocysteine (SAH), which is subsequently hydrolyzed by S-adenosylhomocysteine hydrolase (SAHH) to generate Hcy, is formed when SAM is demethylated during the methyltransferase processes. In order to produce cysteine, Hcy can also join the transsulfuration route, which is mediated by vitamin B6 and cystathionine beta synthase (CBS). Dietary betaine can function as a methyl donor in the liver. Methionine and dimethylglycine (DMG) are produced as a byproduct of the liver enzyme betaine-homocysteine S-methyltransferase (BHMT), which uses betaine from the food as a methyl donor and B6 as a cofactor.