Heritable testicular hypoplasia in Nguni (Bos indicus) bulls: vascular characteristics and testosterone production

Abstract

The biased unilateral occurrence of heritable gonadal hypoplasia was investigated by examining the gross- and microanatomy of the testicular artery and vein, testicular blood flow and testicular testosterone secretion in normal Nguni bulls and in Nguni bulls showing unilateral left, unilateral right and bilateral hypoplasia of the testis. A high incidence of branching of the testicular artery was found ipsilateral to hypoplastic testes. The branching occurs a short distance from the dorsal aorta: one branch proceeds to the testis, the other to the ipsilateral kidney. The association between arterial branching to the kidney and ipsilateral hypoplasia of the testis held for both unilaterally left and unilaterally right hypoplastic bulls. Variations in the anatomy of the testicular vein occurred in both normal and hypoplastic bulls but there was no specific association between the variations and ipsilateral hypoplasia. The lumen diameter of the testicular artery or branch correlated with testis mass. Wall thickness of the artery ipsilateral to hypoplastic testes was not different from that in normal bulls, discounting hyperplasia of the endothelium. Total blood flow to the testis correlated with testis mass. The secretion rate of testosterone from hypoplastic testes was lower than that of normal testes but there was no difference when compared on a unit mass basis.

Ectopic KIT Copy Number Variation Underlies Impaired Migration of Primordial Germ Cells Associated with Gonadal Hypoplasia in Cattle (Bos taurus)

“…Yet the same kind of gonadal hypoplasia, as in Northern Finncattle and Swedish Mountain cattle, has not been observed in any mouse studies. Only for the Nguni breed ( Bos indicus x Bos taurus cross) are there reports of a hereditary form of gonadal hypoplasia resembling that form found in Northern Finncattle and Swedish Mountain cattle [24-26]. Interestingly, the Nguni breed also presents the colour-sided phenotype.…”

Effect of surgical restriction of growth of the testicular artery on testis size and histology in bulls

“…However, with respect to the shape of the tubules, the two types of testis were not comparable. Although these similarities do not prove unequivocally that hypoplasia (heritable) of the testes is due to a restriction of a blood vessel, in the light of the deviations from normal vascularity observed by Kay et al (1992), vascular anomalies may be a cause of hypoplasia. Assuming that the testicular tissue of a bull fetus, homozygous for testicular hypoplasia, is homogeneous and is distributed between the two testes, it is difficult to explain the often asymmetrical manifestation of this condition.…”

“…The animals were weighed at the same time. After 578 days, the bulls were killed and testicular tissue from these animals and from bulls with heritable testicular hypoplasia, described by Kay et al (1992), was fixed in 10% formalin, sectioned and stained with Ehrlich's haematoxylin and eosin. No correction was made for tissue shrinkage as all samples were treated in the same way.…”

“…Hypoplasia of the testis of Nguni bulls has been associated in some instances with anomalies of the testicular artery and in others with decreased total blood flow to the testes (Kay et al, 1992). Molina et al (1985) showed that partial occlusion of a uterine blood vessel resulted in a reduction in the mass of tissue supported by that vessel.…”

Descriptive and cytogenetic study on testicular hypoplasia in a buffalo bull

“…Also, the lower serum testosterone concentration in the bull with testicular hypoplasia compared with normal bulls explains the presence of both feminine characters and low libido. Such low serum testosterone concentration may be attributed to the lower rate of testosterone production by the hypoplastic testes compared with the normal ones [18]. Veeramachaueni et al, [19] attributed the lowered serum testosterone concentration in bulls with testicular hypoplasia to the impairment in the function of the Leydig's cells by local factors either causing tubular damage or those consequent to the tubular damage.…”