Abstract
Vitamin B6 (B6) has a central role in the metabolism of amino acids, which includes important interactions with endogenous redox reactions through its effects on the glutathione peroxidase (GPX) system. In fact, B6-dependent enzymes catalyse most reactions of the transsulfuration pathway, driving homocysteine to cysteine and further into GPX proteins. Considering that mammals metabolize sulfur- and seleno-amino acids similarly, B6 plays an important role in the fate of sulfur-homocysteine and its seleno counterpart between transsulfuration and one-carbon metabolism, especially under oxidative stress conditions. This is particularly important in reproduction because ovarian metabolism may generate an excess of reactive oxygen species (ROS) during the peri-estrus period, which may impair ovulatory functions and early embryo development. Later in gestation, placentation raises embryo oxygen tension and may induce a higher expression of ROS markers and eventually embryo losses. Interestingly, the metabolic accumulation of ROS up-regulates the flow of one-carbon units to transsulfuration and down-regulates remethylation. However, in embryos, the transsulfuration pathway is not functional, making the understanding of the interplay between these two pathways particularly crucial. In this review, the importance of the maternal metabolic status of B6 for the flow of one-carbon units towards both maternal and embryonic GPX systems is discussed. Additionally, B6 effects on GPX activity and gene expression in dams, as well as embryo development, are presented in a pig model under different oxidative stress conditions.
Highlights
Among various metabolic pathways present in the organism, the metabolism of sulfur- (S)methionine and its seleno- (Se) analogous (Se-methionine) are important because they contribute to protein mass and produce (Se) homocysteine, a key metabolite connecting two fundamental metabolic functions, the one-carbon metabolism and the antioxidative system.The transfer of one-carbon groups, represented by methyl (–CH3), methylene (–CH2–), formyl (–CHO), formimino (–CHNH), and methenyl (–CH=), is involved in the remethylation of (Se) homocysteine to (Se) methionine, as well as related pathways such as the folate cycle and the choline oxidation pathway [1]
Dalto et al [39] reported no effect of B6 on either blood SeGPX activity or glutathione peroxidase (GPX) and selenocysteine lyase (SCLY) gene expression in gilts at 30-days of gestation (Tables 1 and 2), a conditions shown to be of low oxidative stress in this species. These results suggest that under basal oxidative stress conditions, in animals supplemented with Se and B6, neither remethylation nor transsulfuration but Se deposition into proteins is the major route for this mineral
Dalto et al [56] observed that maternal supplementation with OSe plus B6 stimulated 28.8 times more genes than MSe plus B6. These findings suggest that embryos coming from OSe supplemented dams have greater Se-methionine reserves and, are more suitable to go through demethylation steps to Se-homocysteine than are embryos from MSe supplemented dams
Summary
Among various metabolic pathways present in the organism, the metabolism of sulfur- (S). Due to the action of the B6‐dependent and Se‐specific enzyme lyase (SCLY), SeCys loses its organic part and releases selenide. The transmethylation of (Se) methionine is not dependent on B6 [11], the direct impact of this vitamin on the transsulfuration of (Se) homocysteine to (Se) cysteine and the intrinsic relation between these two metabolic pathways make the B6 status of an individual important for the antioxidant system but for the one-carbon pool as well. The present review discusses the impact of B6 on the equilibrium between the synthesis and the consumption of one-carbon units under different oxidative stress conditions, focusing sulfur-related metabolism and Se metabolism and the differences between Se sources both in adults and embryos at 5- and 30-days of gestation using a pig model
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have