Association between Rh and plasma iron binding (transferrin)

Abstract

In order to establish the mechanism involved in the maintenance of the Rh polymorphism and fetomaternal compatibility relationships, we examined a sample of children from the North Area of Santiago (Chile), with respect to their growth and development patterns since 1973. This sample had shown large sib-sib segregation distortions for the Rh system. Metric variables, such as plasma protein fractions and iron, academic performance at the end of the last secondary grade and adult stature, were studied in relation to genetic markers, viz., sex, ABO, Xg, MN, Rh, haptoglobins, phosphoglucomutase, and esterase D, by means of unbalanced one way analyses of variance. Highly significant results were found for Rh phenotypes and total iron binding capacity (TIBC, transferrin). However, plasma iron did not differ significantly among Ph phenotypes. Children with the C (Rh) specificity had higher values of TIBC than non-C or c individuals (P less than 0.00001). Evolutionary considerations regarding iron transport and erythroblastosis, relationships between Rh and the transferrin receptor at the plasma membrane, and the location of the Blym-I oncogene (that shares common sequences with transferrins) close to Rh in chromosome 1 are discussed. Less significant results were found between phosphoglucomutase and stature, gamma globulin level and sex, and academic performance (history) and sex.

Sexual orientation, handedness, sex ratio and fetomaternal tolerance-rejection

“…It is a system that develops during zygote and embryo ontogeny and probably includes the natural immune system and has evolved along with placental mammals phylogeny. In this evolutionary context it is important to remark that in these same studies we found an association between the phenotypes of the Rh system and the plasma iron binding capacity (transferrin) level; phenotypes with CeD haplotype (the most hemolytic one in fetomaternal incompatibility) was associated with the highest iron binding capacity in Chile and Colombia (Valenzuela, Avendaño and Harb, 1991;Valenzuela, Bravo and Alarcon, 1995). Zygotes or embryos communicate to the mother (through some unknown molecular or cellular mechanism in the oviduct or the uterus at the first week of implantation) that his or her genome has a spectrum of genes equal to and different from those of the maternal genome (Valenzuela et al, 1980;1981;Valenzuela, 1985Valenzuela, , 1987Valenzuela, , 1996Valenzuela and Walton, 1985;Lucarini et al, 1995;Szekeres-Bartho, 2002;von Rango, 2008).…”