Replication Pattern of Sertoli Cells in Maturing Rat Testis in Vivo and in Organ Culture1

Steinberger, Anna; Steinberger, Emil

doi:10.1093/biolreprod/4.1.84

Cited by 278 publications

(139 citation statements)

References 9 publications

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“…accord with those of Steinberger & Steinberger (1971), who reported that Sertoli cell replication ceased before 20 days of age both in vivo and in organ cultures. The "small mitoses" observed by Clermont & Perey (1957) that they attributed to immature Sertoli cells were not detected after the 15th day of life.…”

Section: Discussionsupporting

confidence: 89%

“…The presence of cellular receptors to both types of hormones has been clearly established (Parvinen, 1982;Hon et al, 1983), but the role of these hormones on the different morphological and func¬ tional aspects of Sertoli cell maturation remains unclear. During the early postnatal period, the Sertoli cells undergo mitotic divisions that cease before the 20th day of life (Steinberger & Steinberger, 1971;Sanborn et al, 1986), and a series of maturational changes that affect the nucleus and cytoplasm (Fawcett, 1975;Ramos & Dym, 1979;Ritzen et al, 1981). This maturational pro¬ cess is dependent on gonadotrophins (Bressler, 1976;Chemes et al, 1979;Vogel et al, 1983), particularly along the LH-testosterone axis, whereas the role of FSH is dependent on the age and physiological status of the animal (Sanborn et al, 1986).…”

Section: Introductionmentioning

confidence: 99%

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Quantitative analysis of Sertoli cells in neonatally oestrogen-treated rats

Gaytan¹,

Aguilar²

1987

Reproduction

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Summary. On Day 1 of age rats were treated with 500 \g=m\g oestradiol benzoate.Oestrogen-treated rats had increased numbers of Sertoli cells per reference area or volume, whereas the total number of cells per testis was unchanged. The mean nuclear size was significantly smaller in oestrogen-treated rats than in control rats, at 22 and 45 days of age. The volume density of the heterochromatin clumps decreased from 22 to 45 days of age in control rats (68% fall), the decrease being slower in oestrogenized animals (30% fall) during the same period. The differences were significant at 45 days of age only. The relative volume occupied by the nuclear membrane infoldings was significantly less in oestrogenized rats than in control ones at the two ages considered. Nucleolar development was delayed in oestrogen-treated rats, which had lower numbers of nuclear sections showing nucleoli, as well as a decrease in the nucleolar diameter. We suggest that these Sertoli cell alterations are due to the altered gonadotrophin and testosterone concentrations induced by the steroid treatment rather than to a direct effect of oestrogen.

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Section: Discussionsupporting

confidence: 89%

Section: Introductionmentioning

confidence: 99%

Quantitative analysis of Sertoli cells in neonatally oestrogen-treated rats

Gaytan¹,

Aguilar²

1987

Reproduction

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“…Thereafter, proliferation slows down and ceases in pups on day 15 after birth (54)(55)(56). It is also known that FSH stimulates Sertoli cell proliferation (56)(57)(58). Fetuses have high circulating concentrations of FSH during the late fetal stage (59,60).…”

Section: Discussionmentioning

confidence: 99%

The masculinization of the fetus during pregnancy due to inhalation of diesel exhaust.

Watanabe¹,

Kurita²

2001

Environ Health Perspect

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This study was conducted to determine the impact of diesel exhaust inhalation on the fetus. Seventy-two pregnant rats and 18 nonpregnant rats were divided into three groups: a group exposed to total diesel engine exhaust containing 5.63 mg/m(3) particulate matter, 4.10 ppm nitrogen dioxide, and 8.10 ppm nitrogen oxide; a group exposed to filtered exhaust without particulate matter; and a group exposed to clean air. The exposure period was from day 7 until day 20 of pregnancy. In addition, 15 pregnant rats were treated with aromatase inhibitors or testosterone to clarify the process by which diesel exhaust exerts its toxicity. The anogenital distance was significantly longer in male and female fetuses from both exhaust-exposed groups than in those of the control. Differentiation of the testis, ovary, and thymus was delayed and disturbed. Maternal testosterone and progesterone levels, which increased due to pregnancy whether or not the rats were exposed, were significantly higher and lower, respectively, in the pregnant rats exposed to total exhaust and filtered exhaust. The serum adrenocorticotropic hormone (ACTH) level and urinary excretion of 17-hydroxycorticosteroids (OHCS) did not differ among the pregnant groups. These results indicate that elevated testosterone did not result from elevated maternal adrenal function. The feto-placental-ovarian unit and inhibition of aromatase activity and synthesis caused by diesel exhaust inhalation might have played an essential role in the accumulation of testosterone. Since both exhaust-exposed groups showed almost the same reactions toward the inhalation, the gaseous phase must have included the relevant toxicants.

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“…Receptors for LH are first detected in the rat fetal testis at 15-5 days and achieve maximal con¬ centration at birth (Warren, Huhtaniemi, Tapanainen, Dufau & Catt, 1984 (Pelliniemi & Dym, 1980), during the late fetal period in rats under the influence of FSH (Orth, 1984) and is wellestablished at birth and then declines in early postnatal life (rat: Steinberger & Steinberger, 1971;Nagy, 1972;lamb: Courot, 1971;Hochereau-de Reviers & Courot, 1978).…”

Section: Prenatal Developmentmentioning

confidence: 99%