A study of glutathione reductase (GR) activity and its stimulation by flavin adenine dinucleotide (FAD) in erythrocytes of Malaysian newborns and adults of different racial groups showed that GR stimulation by FAD was greater than 20% in 50% of 866 newborns (57% of Malays, 55% of Indians and 41% of Chinese) and 54% of 274 adults (46% of Malays, 65% of Indians and 45% of Chinese). There was a significant negative correlation between GR activity and percentage FAD stimulation in both newborns and adults in all racial groups. Low GR activity and a high percentage FAD stimulation were more prevalent among parents of newborns with low GR activity than among parents of newborns with higher GR activity. Administration of riboflavin to mothers with low GR activity resulted in increased GR activity and a decreased percentage of FAD stimulation. None of the individuals examined had clear clinical manifestations of riboflavin deficiency. It is concluded that subclinical riboflavin deficiency leading to low GR activity is prevalent in Malaysia among adults and newborns, especially among Malays and Indians.
Compared with US or European countries, there are fewer mental health services for mothers of children with developmental disabilities in Latin American and/or Southeast Asian countries.
The white blood cell DNA of 36 cord blood samples with Hb Bart's in the red blood cells was studied for alpha-globin gene deletions by hybridization of DNA fragments digested by the restriction endonucleases Eco RI, Hpa I, Bam HI, and Bgl II. All 16 DNA samples from cord blood with Hb Bart's below 3% and no other abnormal hemoglobin had one alpha-globin gene deletion (alpha thal2), except one which had two alpha-globin gene deletions (alpha thal1). Most of the alpha thal2 were of the rightward deletion alpha thal2 genotype. Two new types of alpha thal2 variation was found, probably due to a polymorphism somewhere in an area outside the alpha-globin gene. All 14 cases with Hb Bart's between 3.5% and 8.5% and no other abnormal hemoglobin had two alpha-globin gene deletions (alpha thal1), except one that did not have any alpha-globin gene deletion and one that had one alpha-globin gene deletion. Three DNA samples of cord blood with Hb Bart's accompanied by Hb CoSp did not have any alpha-globin gene deletion. Sixty-five DNA samples from cord blood without Hb Bart's or other abnormal hemoglobin had no alpha-globin gene deletions, except one that had one alpha-globin gene deletion (alpha thal2). Two of the 65 DNA samples were found to have triplicated alpha-globin gene loci.