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The second generation descended from rats treated either with cyclophosphamide alone or with both cyclophosphamide and vinblastine were investigated. As in the first generation, the offspring were evaluated for mean litter size, sex ratio, frequency of gross external malformations and, within the first 4 months of life, growth and mortality. When they reached adulthood, between 12 and 16 weeks of age, the offspring were also tested for spontaneous activity and learning capacity. At birth, the progeny of the treated grandfathers did not show malformations or any other obvious disorder. However, when compared with the control population, the experimental animals showed significantly decreased success rates in a learning task, whatever the learning performance of their parents. Furthermore, decreased spontaneous activity was observed in the male subjects from unsuccessful parents. The similarities between the anomalies found in the first and the second generations argue for the induction of mutations by antimitotic drugs. This hypothesis and the subtle differences between generations and between sexes are discussed.

In the mouse, offspring born from mature fathers exhibit better behavioural performances (for spontaneous activity in both sex and learning capacity in males) than those born from post-pubescent fathers. These behavioural variations are not accompanied by other obvious modifications. They could correspond to what has been observed in man relating to the results in a psychometric test undergone by male progeny born from very young to mature fathers. These data and those which show a decrease in mental performance in rats and human males born from mature to senescent fathers suggest the participation of some genetic factors in these phenomena.

A light microscopic study was carried out on testicular aging in the Wistar rat at the ages of 7, 12, 24, 40, 56, 72, 104, and 124 weeks. The following tissular modifications were observed: a progressive decrease in capillary density, a gradually reduced spermatogenic production, and a progressive increase of degenerating tubular areas. The following two questions were raised: (1) Are the vascular modifications responsible for the other alterations? (2) Do the anomalies inducing a decreased number of spermatozoa simultaneously lead to genetic alterations in the morphologically normal spermatozoa with fertilizing ability? This question is particularly interesting owing to our current knowledge of the consequences of the father's age on offspring.

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