Head hair concentrations of zinc, copper, manganese, alid iron from a total of 418 subjects (154 male and 264 female) aged between 6 mo and 20 yr were measured mainly with flameless atomic absorption spectrophotometry. Only zinc analysis of a part of the female samples (n = 140) were analyzed with inductively coupled plasmaatomic emission spectrometry. The two analytical methods showed close agreement. The mean concentration of copper and manganese were significantly higher in male subjects than in female subjects. The trace element concentrations in hair varied with the subject's age. Zinc concentration in hair decreased from 6 mo to 14 yr in the male subjects and decreased from 6 mo to 12 yr in the female subjects. Then, the concentrations increased gradually to 20 yr in the both sexes. Age-dependent variations of copper and manganese concentrations in hair showed similar trends to those of zinc. The results of this study suggest that a higher concentration in the diet of these trace elements may be required for growing children, especially in the period of adolescence.
The adsorption of zinc and lead on hair was dependent on the acidity of the hair and/or the medium in which the hair sample was immersed, suggesting that hair is an ion exchanger. The pKa was estimated to be between 4.5 and 5.0. The coexistence of mercuric ion or PCMB reduced zinc adsorption by only a few percent, whereas zinc inhibited mercuric ion adsorption to a greater extent. These facts suggest that the binding sites in hair for metals are located on functional groups like carboxyl groups rather than sulfhydryl groups. The removal and/or elution of metals from hair were observed for 18 elements by various washing procedures. By treating hair with a water solution of detergent, alkaline metals were eluted to a great extent, whereas alkaline earth metals were eluted to some extent. The other metals did not vary with any procedures tested.
Sodium dichloroacetate (DCA) was administered orally at a dose of 50 mg per kg body weight twice or three times per day to a newborn infant with lactic acidosis of unknown cause (patient 1) and to a 15-year-old boy with mitochondrial encephalomyopathy associated with lactic acidosis (patient 2). In patient 1, during treatment with DCA, DCA accumulated in the blood judging from the findings that the urinary excretion of DCA increased cumulatively and the blood lactate level rapidly decreased to the normal range. In patient 2, the blood DCA level gradually increased during treatment to a concentration of 250 micrograms ml-1 and the blood lactate level decreased and was maintained within the normal range. DCA was detected in the brain (25 micrograms g tissue-1) and the liver, kidney and muscle (33.8, 33.8 and 26.3 micrograms g tissue-1, respectively) obtained at autopsy of patient 1, and in the cerebrospinal fluid of patient 2 at a concentration of 125 micrograms ml-1 when the blood concentration was 250 micrograms ml-1. The lactate levels in the cerebrospinal fluid decreased from 7 and 4 mmol l-1 to 2.4 and 2.6 mmol l-1 in patients 1 and 2, respectively. Thus DCA may be useful in clinical treatment of chronic congenital lactic acidosis because it seems to cross the blood-brain barrier. However, it must be given at non-toxic doses, determined by monitoring the concentrations of lactate and DCA in the blood, because orally administered DCA tends to accumulate in tissues.
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