No abstract

Summary. The role of ascorbic acid in the metabolism of storage iron was investigated in guinea‐pigs. Ascorbic acid deprivation increased the total non‐haem iron concentration in the spleen and reduced it in the liver, and in both organs ferritin was diminished and haemosiderin increased. Replacing the ascorbic acid restored the normal distribution of iron between the two storage compounds, and in the spleen the total storage iron concentration returned to control levels within 24 hr. Evidence was obtained in experiments with 59Fe that the accumulation of iron in the spleen was due to a diminished release from reticulo‐endothelial cells. When 59Fe‐labelled haemoglobin in denatured red cells was injected, release of the isotope was inhibited in scorbutic animals. In contrast, after injecting labelled transferrin, 59Fe in the liver parenchymal cells was released to a greater extent than in normals. These observations may explain certain ferrokinetic peculiarities in patients with scurvy, and possibly also the predominantly reticulo‐endothelial localization of the iron in Bantu subjects with siderosis.

The prevalence of heterozygous familial hypercholesterolemia was determined in a representative sample of 403 young Jewish men resident in Johannesburg, South Africa. Preliminary screening by measurement of serum total cholesterol demonstrated that 25 of them had levels greater than or equal to 7.5 mmol/l (290 mg/dl). On the basis of subsequent clinical, biochemical, and family studies, 6 men, or about 1 in 67 of the total sample, were considered to be heterozygotes. This very high prevalence, about 7 times greater than that found in other Caucasian populations, is probably related to founder effect. It may help to explain the high frequency of coronary heart disease in Johannesburg Jews.

No abstract