Biomedical Engineering Reference
In-Depth Information
Fig. 9.3
Diagrammatic representation of time courses of changes in relative sperm counts in dif-
ferent species. Rodent data are based on testicular and epididymal counts; the primate data on
ejaculated sperm counts. Note the different time scales in rodents and primates. The durations of
a single cycle of the seminiferous epithelium in each species are given in parentheses. The data
were obtained in mice (Meistrich et al.
1978
; Meistrich and Samuels
1985
; Searle and Beechey
1974
), Sprague-Dawley rats (Dym and Clermont
1970
; Velez de la Calle JF et al.
1989
), LBNF
1
rats (Kangasniemi et al.
1996b
; Meistrich et al.
2001
), macaques (Kamischke et al.
2002
) and
human single dose (Rowley et al.
1974
) and fractionated (Fx) (Dubey et al.
2000
; May et al.
2000
)
irradiations
The effects of gonadotoxic therapies on the somatic cells of the testis and on the
hypothalamic-pituitary-gonadal axis are not immediate and generally appear to be
secondary to the loss of germ cells. Germ cell loss causes reduced inhibin secretion
by the Sertoli cells, resulting in increased follicle-stimulating hormone (FSH) secre-
tion by the pituitary (Boekelheide and Hall
1991
). Testosterone production is usually
unaffected, but germinal aplasia reduces testis size and consequently testicular blood
flow, resulting in less testosterone being distributed into the circulation (Wang et al.
1983
) and hence increased luteinizing hormone (LH) secretion by the pituitary.
9.3
Stem Spermatogonial Survival-Methods
Regeneration of spermatogenesis requires the survival of spermatogonial stem
cells. Several different approaches have been taken to assess their survival.
Morphological criteria have been used to quantify numbers of putative sper-
matogonial stem cells. In rodents, it is generally accepted that isolated undifferenti-
ated type A spermatogonia, designated A
s
, are the stem cells (Huckins
1971a
). When
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