Experiment 1088917
Details
| Property | Value |
|---|---|
| Pharmacology | |
| Administration route | SC |
| Organism | Empty organism |
| Citation | OKO,R: HRUDKA,F:. (1982). EFFECT OF GOSSYPOL ON SPERMATOZOA.. 3(3) |
| Amount utilized | |
| Compound isolated | |
| Disease | DAILY DOSING FOR 30 DAYS. RESPONSES WERE MONITERED MICROSCOPICALLY ON SPERM EXTRACTED FROM TESTIS,AND PROXIMAL,MIDDLE AND DISTAL EPIDIDYMIS AT REGULAR INTERVALS,DURING AND AFTER TREATMENT,UP TO 70 DAYS ULTRASTRUCTURAL CHANGES WERE EVALUATED ON SPERM IN SITU BY PERFUSION. THE EFFECT ON SPERMATOGENESIS WAS ASSESSED QUALTITATIVELY AND QUANTITATIVELY IN ANIMALS TREATED FOR 18 AND 30 DAYS AT THE SPERM LEVEL,GOSSYPOL HAD A SPECIFIC EFFECT ON THE MITOCHANDRIAL APPARATUS THAT WAS EXPRESSED IN THE FORM OF SEGMENTAL APLASIA,WHICH OCCURRED PREDOMINANTLY JUST ABOVE THE ANNULUS AND IN DEGENERATIONOF INDIVIDUAL MITOCHANDRIA. THE APLASIA WAS THE ONLY DEFECT RECOGNIZED IN SPERM EXTRACTED FROM TESTIS AND PROXMAL EPIDIDYMIS. DISLOCATIONS OF AXIAL FIBERS WERE OBSERVED AND PROGRESSIVELY INCREASED DURING EPIDIDYMAL TRANSIT. THESE SECONDARY LESIONS LED TO ERRATIC MOVEMENT AND FERTILITY LOSS. PROLONGED TREATMENT INHIBITED MOTILITY COMPLETELY. MITOCHONDRIAL DEGENERATION WAS FIRST RECOGNIZED IN STEP 18 OF SPERMIDGENESIS,A TIME WHEN THE DEVELOPMENT OF THE MITOCHONDRIAL SHEATH IS ALMOST COMPLETE IT CONTINUED BEYOND SPERMIATION AND WAS AGGRAVATED BY PROLONGATION OF TREATMENT. SUCH A DEGENERATION WAS NOT OBSERVED IN PRECEEDING STEPS OF SPERMATIDS,NOR IN PRECURSORS AND SERTOLI CELLS. APLASIA WAS THE RESULT OF MITOCHONDRIAL DEFICIT CAUSED BY MITOCHONDRIAL DEGENERATION. |
| Dose amount | 20.0 MG |
| Number | 1 |
| Qualitative result | ACTIVE |
| Animal | RAT |
| Per unit | KG |
| Dose expression | DOSE |
| Gender | MALE |