Changes in the rat lymphoid tissues after Leydig cell destruction by ethane-1,2-dimethanesulphonate

Leeming, G.; Lendon, R. G.; McLean, John M.; Morris, Ian D.

doi:10.1016/s0232-1513(11)80008-3

Cited by 4 publications

(1 citation statement)

References 25 publications

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“…On the other hand, during the 15-day period after EDS administration the regenerative process might already have started, since adrenal weight is fully restored 30 days following injection (Ple}a{ et al 2001). In almost all biological systems affected by EDS the nature of the changes has been found to be transitory; for instance, thymic weight recovers by 7 days after injection of EDS (Leeming et al, 1991). A compensatory stimulation of the inner zone might also occur.…”

Section: Resultsmentioning

confidence: 99%

The effects of acth, isoproterenol and Dexamethasone on the rat adrenal gland response to ethane dimethanesulphonate (Eds): A stereological study

Plećaš-Solarović¹,

Pešić²,

Mirković³

et al. 2003

Acta vet. (Beogr.)

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Ethane dimethanesulphonate (EDS), an alkylating agent, caused marked atrophy of the adrenal cortex of adult male rats, in addition to its toxic effect on testicular Leydig cells. The aim of this work was to examine whether a 9-day treatment with ACTH (40 IU/kg/d), isoproterenol (120 mg/kg/d) or dexamethasone (0.25 mg/kg/d), which started 4 days prior to intraperitoneal administration of a single dose of EDS (75 mg/kg), affected the morphological changes in the adrenal cortex evoked by EDS alone. The animals were killed 15 days after EDS injection. Stereological analysis revealed that both ACTH and isoproterenol almost completely prevented cortical atrophy induced by EDS. They also considerably stimulated corticosterone secretion in EDS-injected animals. By contrast, in dexamethasone-suppressed rats, the deleterious effect of EDS on adrenocortical cells was augmented. The volume and cellularity of all cortical zones were reduced, but the remaining cells of the zona reticularis displayed considerable hypertrophy which was probably responsible for the maintenance of corticosterone secretion. These results clearly demonstrate that both ACTH and b adrenoceptor stimulation have protective action against the toxic effects of EDS on rat adrenal cortex, whereas dexamethasone exerts an opposite influence

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Section: Resultsmentioning

confidence: 99%

The effects of acth, isoproterenol and Dexamethasone on the rat adrenal gland response to ethane dimethanesulphonate (Eds): A stereological study

Plećaš-Solarović¹,

Pešić²,

Mirković³

et al. 2003

Acta vet. (Beogr.)

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Leydig Cell Apoptosis in Response to Ethane Dimethanesulphonate After Both In Vivo and In Vitro Treatment

MORRIS,

TAYLOR,

MORRIS

1997

Journal of Andrology

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The biological effects of ethane dimethanesulphonate (EDS) are unique since cytotoxicity in the adult rat is almost exclusively confined to the Leydig cells. For this reason, EDS has been used extensively to investigate the physiological role of the Leydig cell and its products. Experiments were conducted to determine whether the Leydig cell will undergo apoptosis in response to EDS or methylprednisolone (MP), a glucocorticoid known to cause apoptosis in a number of other cell types. Percoll‐purified Leydig cells were incubated for 24 hours with EDS (750 μg/ml), at which time the cells attached to the culture plate became rounded up while control cells were flattened and polyhedral. Following incubation with EDS or MP (10 μM), cells that became detached from the plate were characteristically apoptotic when stained with the fluorescent DNA dye, acridine orange. These cells had shrunk and the nuclear chromatin had become condensed, which is an early characteristic of apoptosis in other cells; eventually, apoptotic bodies formed, reflecting a later apoptotic stage. Electrophoresis of DNA extracted from the treated Leydig cells exhibited the characteristic ladder of the apoptotic process. Increasing the concentration of EDS or MP resulted in a dose‐dependent increase in the incidence of apoptosis that reached a maximum of 25% (EDS) or 12% (MP) of detached cells. Administration of EDS in vivo caused a 20‐fold increase in the number of apoptotic cells observed in interstitial cell preparations. In conclusion, the data indicates that programmed cell death, apoptosis, can occur in the Leydig cell and that this is the likely mechanism by which EDS kills the cells in vivo and in vitro.

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Thymic regression and apoptosis in the rat after treatment with the Leydig cell cytotoxin ethylene dimethanesulphonate (EDS)

et al. 1997

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Changes in the rat lymphoid tissues after Leydig cell destruction by ethane-1,2-dimethanesulphonate

Cited by 4 publications

References 25 publications

The effects of acth, isoproterenol and Dexamethasone on the rat adrenal gland response to ethane dimethanesulphonate (Eds): A stereological study

The effects of acth, isoproterenol and Dexamethasone on the rat adrenal gland response to ethane dimethanesulphonate (Eds): A stereological study

Leydig Cell Apoptosis in Response to Ethane Dimethanesulphonate After Both In Vivo and In Vitro Treatment

Thymic regression and apoptosis in the rat after treatment with the Leydig cell cytotoxin ethylene dimethanesulphonate (EDS)

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