Oxidative stress in mothers who have conceived fetus with neural tube defects: the role of aminothiols and selenium.
OBJECTIVE
Methionine metabolic impairment and selenium deficit have been associated to neural tube defects. The relationship between thiol metabolism and selenium is not well known. We assessed the status of aminothiols and selenium, as well as thiolic status and the amino acids involved in arginine synthesis in the case of selenium depletion and repletion, studying their relationship to neural tube defects.


METHODS
We studied 44 women of 37 +/- 8 years (mean +/- SD) who had conceived fetuses with neural tube defects as cases; and 181 women of 39 +/- 7 years (mean +/- SD) with healthy children as controls. We determined selenium, vitamin B12, serum folates, plasma thiol compounds and amino acids. Homocysteine transsulfuration was assessed using total cysteine/total homocysteine ratio (tCys/tHcy), and selenium repletion cut-off value was 1.06 micromol/l (84 microg/l).


RESULTS
Cases showed significantly lower levels (median) than controls of total homocysteine (P = 0.001), total cysteinylglycine (P < 0.001), selenium (P < 0.001) and tryptophane (P = 0.002); and higher tCys/tHcy levels (P < 0.001), glutathione (P = 0.008) and L-arginine (P = 0.001). Cases with selenium depletion (selenium < or = 1.06 micromol/l) had significantly higher levels than controls of cysteine (P = 0.010), glutathione (P = 0.005), tCys/tHcy (P < 0.001), and arginine (P = 0.004), but significantly lower levels than controls of tryptophane (P = 0.027), cysteinylglycine (P < 0.001) and folates (P < 0.001). Only cysteinylglycine was lower than controls (P < 0.001) when selenium > 1.06 micromol/l. Methionine levels were higher in cases with selenium depletion than in repletion (P = 0.029).


CONCLUSIONS
According to our data, a diet deficient in selenium and folates or their absorption impairment, and/or other mechanisms related to polyamines and nitric oxide can lead to oxidant/antioxidant imbalance and to a higher occurrence of these malformations.
Martín
Inmaculada
I
Servicio de Análisis Clínicos, Hospital Universitario Son Dureta, Andrea Doria 55, Palma de Mallorca 07014, Spain. imartin@hsd.es
Gibert
Ma José
MJ
Pintos
Concepción
C
Noguera
Aina
A
Besalduch
Antoni
A
Obrador
Antoni
A
D000328:Adult; D016022:Case-Control Studies; D003545:Cysteine / Q000097:blood / Q000378:metabolism; D004151:Dipeptides / Q000097:blood / Q000378:metabolism; D005260:Female; D005492:Folic Acid / Q000097:blood / Q000378:metabolism / Q000502:physiology*; D005978:Glutathione / Q000097:blood / Q000378:metabolism; D006710:Homocysteine / Q000097:blood / Q000378:metabolism*; D006801:Humans; D007231:Infant, Newborn; D008715:Methionine / Q000378:metabolism / Q000502:physiology; D009035:Mothers / Q000523:psychology*; D009436:Neural Tube Defects / Q000097:blood / Q000209:etiology* / Q000378:metabolism; D010084:Oxidation-Reduction; D018384:Oxidative Stress / Q000502:physiology*; D012643:Selenium / Q000172:deficiency / Q000378:metabolism / Q000502:physiology*; D013438:Sulfhydryl Compounds / Q000378:metabolism / Q000502:physiology*
D004151:Dipeptides; D013438:Sulfhydryl Compounds; D006710:Homocysteine; C028505:cysteinylglycine; D005492:Folic Acid; D008715:Methionine; D005978:Glutathione; D012643:Selenium; D003545:Cysteine