The present study aims to define, characterize and compare the long-term ef
fects on offspring of delayed parenthood. Data published so far on this top
ic show that maternal and paternal ageing may affect offspring by different
mechanisms. Delayed motherhood is characterized by increased probability o
f obstetric complications and/or fetal and perinatal problems which, in tur
n, may increase the risks of mortality and morbidity in newborns and later
life. Furthermore, maternal ageing is distinguished by a decreased ratio of
male to female infants and higher odds of conceiving a trisomic child and/
or an individual suffering from mitochondrial DNA disorders. In contrast, d
elayed fatherhood is associated with higher risks of conceiving an individu
al suffering from new inheritable-mutation disorders. The different pattern
of disease in offspring associated with maternal and paternal ageing may b
e explained, among other factors, by the fact that (i) oocytes of middle-ag
ed women may suffer oxidative stress because their mitochondria produce hig
her amounts of reactive oxygen species; (ii) diplotene oocytes and to a les
ser extent metaphase I and II oocytes have an efficient DNA repair system w
hich is essentially independent of maternal age; and (iii) mitochondria are
transmitted to the next generation along the matrilineal line. Moreover, (
i) the activities of antioxidant enzymes within the seminal plasma and sper
matozoa from older men may be reduced and so spermatozoa may be more vulner
able to mutational changes than spermatozoa from younger men; and (ii) late
spermatids, and immature,and mature spermatozoa do not have a DNA repair s
ystem.