Ontogeny of hepatic methionine catabolic enzyme activities (Transmethylation and Transsulphuration) and associated physiological amino acids in E10‐21 chick embryos and D1‐49 broilers

Jin, Lü; Weil, Jordan; Cerrate, S.; Coon, C. N.

doi:10.1111/jpn.13463

Cited by 2 publications

(4 citation statements)

References 44 publications

(113 reference statements)

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“…(1996) reported that a vitamin B 6 deficiency may contribute to impaired transsulfuration in humans, in accordance with the response of plasma concentration of homocysteine, cystathionine, and cysteine after a methionine load. The finding of unchanged cysteine (M + 3/M + 0) in 18-day-old chick embryos from breeders fed without pyridoxine supplementation may be attributed to a limited transsulfuration ability in chick embryos suggested by Lu et al., 2020a , Lu et al., 2020b . Moreover, in accordance with the dissociation constants of CBS (0.7 umol/L) and SHMT (27.5 umol/L) ( Jones and Priest, 1978 ; Kery et al., 1999 ), it seems that during vitamin B 6 deficiencies, the SHMT can be affected, but little or no effect on CBS is observed.…”

Section: Discussionmentioning

confidence: 94%

“…The synthesis of cysteine from serine and homocysteine via transsulfuration pathway is catalyzed by cystathionine ß-synthase (EC 4.2.1.22) and cystathionase, and both of these enzymes require vitamin B 6 . Lu et al. (2020b) recently reported lower levels of cystathionine ß-synthase in the E10-E21 embryo liver and from day 1 to day 7 in the liver of hatched chicks compared with cystathionine ß-synthase in 35 to 49 d broilers.…”

Section: Discussionmentioning

confidence: 95%

“…Owing to its involvement in metabolic processes and oxidative stress, a nutritional imbalance of methionine can lead to a variety of metabolic problems. For instance, prior studies have suggested that altered methionine supplies impair normal methionine metabolism in laying hens and broilers and methionine metabolism plays an important role in chick embryo growth and development ( Cao et al., 1995 ; Lu et al., 2020a , 2020b ). In addition, Rosenquist and Finnell reported that increased homocysteine levels impaired chick embryonic development.…”

Section: Introductionmentioning

confidence: 99%

“…In addition, Rosenquist and Finnell reported that increased homocysteine levels impaired chick embryonic development. In separate studies with chick embryos and broiler chicks hatched from breeders fed control nutrient and vitamin formulations, Lu et al., 2020a , Lu et al., 2020b , Stipanuk, 2004 indicated lower levels of cystathionine ß-synthase activity may be limiting cysteine formation during embryogenesis and during the early period of broiler grow-out. High levels of cystathionine found in the human fetus have been shown to be related to a limitation of the transsulfuration pathway because the cystathionase (EC 4.4.1.1, C-ase) activity does not appear until after birth ( Gaull et al., 1972 ).…”

Section: Introductionmentioning

confidence: 99%

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The effect of feeding adequate or deficient vitamin B6 or folic acid to breeders on methionine metabolism in 18-day-old chick embryos

et al. 2021

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Three isotopic tracers ([2,3,3- 2 H 3 ]-L-serine, [ 2 H 11 ]-L-betaine, and [1- 13 C]-L-methionine) were administered by amnion injection into 18-day-old chick embryos to investigate the kinetics of methionine metabolism. The embryos utilized were from eggs collected from 34-week-old Cobb 500 broiler breeders that were fed either a control diet containing folic acid (1.25 mg/kg diet) and pyridoxine HCl (5 mg/kg diet) or diets devoid of supplemental pyridoxine or folic acid. Intermediate metabolites of methionine metabolism and polyamines were analyzed in 18-day-old chick embryos. There were no differences in hepatic [ 2 H 2 ] methionine or [ 2 H 3 ] cysteine enrichments or in physiological concentrations of sulfur amino acids for chick embryos from breeders fed the control diet and embryos from breeders fed diets containing no pyridoxine or folic acid. Supplementation of B 6 or folic acid did not affect the production of methionine and cysteine in chick embryos. However, breeders fed the control diet with both folic acid and pyridoxine supplementation produced embryos with a two-fold reduction of hepatic homocysteine and increased spermine compared with embryos from breeders fed diets containing no supplemental pyridoxine or folic acid ( P < 0.05). Hepatic S-adenosylmethionine for embryos from breeders fed no supplemental B 6 was half the concentration compared with embryos from breeders fed the control diet. Embryos from breeders fed the control diet were utilized to determine the proportion of homocysteine going through remethylation and transsulfuration and also to determine the pathway of remethylation. Sixty-five percent of the methyl groups used for homocysteine remethylation from control embryos was via the MFMT pathway. Alternatively, 61% of homocysteine from control embryos was remethylated via the MFMT and the BHMT reactions and 39% of homocysteine was catabolized to cysteine via the transsulfuration pathway. These data show that in embryos, intermediate metabolites of methionine and polyamines increase in concentration when pyridoxine levels are provided in deficient concentrations to the breeder hen. In addition, this research demonstrates that folic acid deficient embryos conserve methionine, rather than catabolize it to cysteine.

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