Maternal seafood consumption is associated with improved selenium status: Implications for child health

被引:6
作者
Ralston, Nicholas V. C. [1 ,6 ]
Raymond, Laura J. [2 ]
Gilman, Christy L. [3 ]
Soon, Reni [4 ]
Seale, Lucia A. [5 ]
Berry, Marla J. [5 ]
机构
[1] Univ ND, Earth Syst Sci & Policy, Grand Forks, ND USA
[2] Sage Green Nutr Res Guidance, Grand Forks, ND 58203 USA
[3] Univ Virginia, Sch Med, Div Gastroenterol & Hepatol, Charlottesville, VA 22903 USA
[4] Univ Hawaii Manoa, Dept Obstet & Gynecol, Honolulu, HI 96813 USA
[5] Univ Hawaii Manoa, Pacific Biosci Res Ctr, Honolulu, HI 96822 USA
[6] Univ North Dakota, Earth Syst Sci & Policy, 312 Clifford Hall, Grand Forks, ND 58202 USA
基金
美国海洋和大气管理局;
关键词
Selenium; Mercury; Cord blood; Placenta; Pregnancy; Seafood; Ocean fish; PRENATAL METHYLMERCURY EXPOSURE; APOLIPOPROTEIN-E RECEPTOR-2; METHYL MERCURY EXPOSURE; TRACE-ELEMENTS INTAKE; FISH CONSUMPTION; NEURODEVELOPMENTAL OUTCOMES; THIOREDOXIN SYSTEM; FAROE-ISLANDS; MOLAR RATIOS; MAIN COHORT;
D O I
10.1016/j.neuro.2024.01.003
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Selenium (Se) is required for synthesis of selenocysteine (Sec), an amino acid expressed in the active sites of Sedependent enzymes (selenoenzymes), including forms with essential functions in fetal development, brain activities, thyroid hormone metabolism, calcium regulation, and to prevent or reverse oxidative damage. Homeostatic mechanisms normally ensure the brain is preferentially supplied with Se to maintain selenoenzymes, but high methylmercury (CH3Hg) exposures irreversibly inhibit their activities and impair Sec synthesis. Due to Hg's high affinity for sulfur, CH3Hg initially binds with the cysteine (Cys) moieties of thiomolecules which are selenoenzyme substrates. These CH3Hg-Cys adducts enter selenoenzyme active sites and transfer CH3Hg to Sec, thus irreversibly inhibiting their activities. High CH3Hg exposures are uniquely able to induce a conditioned Sedeficiency that impairs synthesis of brain selenoenzymes. Since the fetal brain lacks Se reserves, it is far more vulnerable to CH3Hg exposures than adult brains. This prompted concerns that maternal exposures to CH3Hg present in seafood might impair child neurodevelopment. However, typical varieties of ocean fish contain far more Se than CH3Hg. Therefore, eating them should augment Se-status and thus prevent Hg-dependent loss of fetal selenoenzyme activities. To assess this hypothesis, umbilical cord blood and placental tissue samples were collected following delivery of a cohort of 100 babies born on Oahu, Hawaii. Dietary food frequency surveys of the mother's last month of pregnancy identified groups with no (0 g/wk), low (0-12 g/wk), or high (12 + g/wk) levels of ocean fish consumption. Maternal seafood consumption increased Hg contents in fetal tissues and resulted in -34% of cord blood samples exceeding the EPA Hg reference level of 5.8 ppb (0.029 mu M). However, Se concentrations in these tissues were orders of magnitude higher and ocean fish consumption caused cord blood Se to increase -9.4 times faster than Hg. Therefore, this study supports the hypothesis that maternal consumption of typical varieties of ocean fish provides substantial amounts of Se that protect against Hgdependent losses in Se bioavailability. Recognizing the pivotal nature of the Hg:Se relationship provides a consilient perspective of seafood benefits vs. risks and clarifies the reasons for the contrasting findings of certain early studies.
引用
收藏
页码:26 / 35
页数:10
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