Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P56851 (epididymal)
 11,273 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of castration and testosterone replacement therapy on the histology and biochemical composition (RNA, DNA, total protein, alkaline phosphatase, acid phosphatase, hyaluronidase, sialic acid, glycogen, phospholipids, and glycerylphosphorylcholine [GPC]) of the epididymis of the rabbit and rhesus monkey were investigated. Castration produced marked ponderal, histologic, and biochemical changes in the epididymis. In the androgen-deficient state the tubular diameter and epithelial cell height were reduced and there was an increase in interbular stroma. The levels of RNA, DNA, phospholipids, and GPC were also reduced in castrated animals. Testosterone treatment restored the histologic features and the levels of various biochemical constituents to a great extent but not to the intact control level. The importance of endocrine and exocrine factors of the testis in relation to epididymal function is discussed.
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PMID:Androgenic control of epididymal function in rhesus monkey and rabbit. 40 58

The specific activities of three acid phosphatases were followed in the epididymis of growing rats. All activities were constantly rising but revealed two steeper parts probably corresponding to the increase of androgen secretion and the arrival of spermatozoa in the epididymis. Simultaneously an increase in the histochemical staining was obtained in all epididymal segments. Both biochemical and histochemical studies showed that castration reduced the activity of all acid phosphatases and this could be restored with testosterone-estradiol treatment. Estradiol had no effect on the activities in the castrated animal, but in the normal animal it caused an elevation of Enzyme I activity. In the histochemical study estradiol seemed to restore the acid phosphatase activity. Enzyme I reacted slower than the others to both castration and hormone treatment. Increased elimination caused by ligation of the epididymis caused a reduction in the activity of all enzymes within four days. It was greatest in the area of the corpus. This study, however, rendered no further elucidation for the assumption that acid phosphatases participate in the elimination of excessive and defective spermatozoa.
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PMID:Acid phosphatase of the rat epididymis. III. Histochemical and biochemical responses in experimental conditions. 59 63

The fine structure distribution of non-specific acid phosphatase was determined in the head region of mouse spermatozoa from the testes, the caput, corpus and cauda epididymidis and the ductus deferens. Enzymatic localization was achieved by the Gomori technique. The postacrosomal dense lamina, the nuclear side of the inner acrosomal membrane and the space between the plasmalemma and the outer acrosomal membrane showed reaction product in spermatozoa from the testis and caput epididymidis. Spermatozoa from the cauda epididymidis exhibited reaction product only between the plasmalemma and the outer acrosomal membrane. Spermatozoa from the corpus epididymidis and from the ductus deferens showed no reaction product in the head region. The changes observed in the distribution of acid phosphatase in the sperm head during epididymal transport may reflect maturational events.
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PMID:Fine structure distribution of non-specific acid phosphatase in the head region of mouse spermatozoa from various regions of the male reproductive tract. 117 Mar 28

The relationship between the antifertility effect of alpha-chlorohydrin and changes in composition of luminal plasma from the cauda epididymidis of rats and rabbits has been investigated. At each dose regimen studied, the fertilizing capacity of rats treated with alpha-chlorohydrin was reduced to zero. The levels of sodium, potassium, glycerylphosphorylcholine (GPC), acid phosphatase and alkaline phosphatase in epididymal plasma were not markedly affected by drug treatment. The most noticeable change was a considerable increase in the concentration of lactic dehydrogenase (LDH) at all dose levels and of glutamic-oxaloacetic transaminase (GOT) after 7 days of treatment with 8 and 16 mg/kg. The effect of cold shock on the composition of epididymal plasma showed that LDH and GOT are, at least in part, derived from spermatozoa. In contrast, alpha-chlorohydrin did not have an antifertility action in the rabbit, and the only notable change in the compositon of epididymal plasma was an increase in the level of GPC. These results provide evidence that, in the rat, alpha-chlorohydrin or a metabolite primarily exerts its antifertility effect by a direct action on the spermatozoa, whilst in the rabbit a barrier may exist to the entrance of the drug into the lumen of the epididymal duct.
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PMID:The effects of alpha-chlorohydrin on the composition of rat and rabbit epididymal plasma: a possible explanation of species difference. 119 43

Effect of styrene (100 or 200 mg/kg body wt/day) for 60 days was observed on testicular enzymes of postnatally maturing rats. A significant decrease in epididymal spermatozoa count was observed only at 200 mg/kg body weight dose. Activities of testicular sorbitol dehydrogenase and acid phosphatase decreased while activities of lactate dehydrogenase, beta-glucuronidase, glucose-6-phosphate dehydrogenase, and gamma-glutamyl transpeptidase significantly increased only in animals exposed to styrene at a dose of 200 mg/kg body weight. The results suggest that exposure to high dose of styrene during developmental period alters the activities of enzymes associated with specific cell type of testis.
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PMID:Effect of styrene on testicular enzymes of growing rat. 145 17

Flutamide, a pure antiandrogen, increases the levels of plasma luteinizing hormone but antagonizes the biological expression of androgen on target organs. Flutamide was administered to rats to study the effect of altered availability of hormones on the functional status of epididymis. The weights of ventral prostate, seminal vesicles and epididymis showed antiandrogenic effects of flutamide. However, increased activity of kidney beta-glucuronidase reflected increased availability of testosterone. The concentrations of protein and DNA along with the activities of acid phosphatase and hyaluronidase decreased in flutamide-treated rats. The activities of acid phosphatase and hyaluronidase in epididymal sperms along with protein concentration increased in flutamide-treated rats. Alteration of epididymal function by treatments affecting lysosomal stability was indicated.
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PMID:Effect of flutamide on the physiological status of epididymis and epididymal sperms. 160

Diabetes mellitus caused significant reduction in serum testosterone and accessory sex glands weight. The sperm content of epididymal regions also decreased. Among the epididymal regions, the cauda epididymidal tissue alone showed significant reduction in Na(+)-K+ ATPase activity. However, Mg2+ ATPase activity was lowered in caput epididymidis only. Specific activity of Ca2+ ATPase significantly decreased in caput and cauda epididymides. All three ATPases decreased significantly in caput epididymidal spermatozoa leaving cauda epididymidal spermatozoa unaffected. Specific activity of alkaline phosphatase was suppressed in caput epididymidis and in the spermatozoa collected from caput and cauda epididymides, while the acid phosphatase was unaffected. In general, the results are suggestive of definite influence of diabetes on epididymal phosphatases which is region specific. Diabetes induced decrease in phosphatases may have an impact on secretory and absorptive functions of epididymis and thus on sperm maturation.
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PMID:Effect of diabetes mellitus on epididymal enzymes of adult rats. 166 46

It is the purpose of this study to determine the effects of Zn deficiency on the biochemical composition of testes, epididymis, and seminal vesicle of rabbits. An attempt is made to evaluate previous physiological studies and to correlate them with biochemical changes. 30 mature male Balady rabbits were used in this study. 1 group was fed a Zn-deficient diet, and 2 control groups were pair-fed or fed ad libitum a Zn-sufficient diet, all for a period of 120 d. There was significant reduction in the levels of hyaluronidase, alkaline phosphatase, acid phosphatase, lactic dehydrogenase, sialic acid, protein, and Zn of both testes and epididymis of Zn-deficient rabbits. Reduction in the level of glyceryl-phosphoryl choline in the epididymis of Zn-deficient rabbits was the best indicator of inhibition of epididymal secretory activity. In contrast, the cholesterol and glycogen contents of the testes were elevated. The results also showed in Zn-deficient rabbits significant reduction in androgen-sensitive parameters, namely fructose and citric acid in the seminal vesicle. Zn levels were decreased in the seminal vesicle. The results indicated that Zn deficiency caused inhibition of testicular, epididymal, and seminal vesicle function and, consequently, caused reductions in the biochemical composition of these organs.
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PMID:Response of testes, epididymis, and seminal vesicle of rabbits to zinc deficiency. 178 25

In utero exposure to di(2-ethylhexyl)phthalate (DEHP; 1000 mg/kg body weight) significantly decreased activities of testicular sorbitol dehydrogenase and acid phosphatase and increased gamma-glutamyl transpeptidase, lactate dehydrogenase and beta-glucuronidase activities at early ages. A decrease in the sperm count of the epididymal spermatozoa was also observed in the sexually matured animals of DEHP exposed group. The data suggest that in utero exposure to DEHP may affect the normal development of testes.
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PMID:Effect of in utero exposure to di(2-ethylhexyl)phthalate on rat testes. 181 82

Di-n-butyl phthalate (DBP) was administered to adult male rats by gavage at the doses of 250, 500 and 1000 mg/kg body weight/day for 15 days. A significant decrease in epididymal spermatozoa counts was observed at 500 and 1000 mg/kg doses of DBP. The activity of sorbitol dehydrogenase was found to be significantly decreased while that of lactate dehydrogenase, gamma-glutamyl transpeptidase, beta-glucuronidase, and glucose-6-phosphate dehydrogenase, significantly increased in the animals exposed to 500 and 1000 mg/kg of DBP. Decrease in the activity of acid phosphatase was also observed at all dose levels. Histopathological studies revealed marked degeneration of seminiferous tubules, further confirming testicular toxicity of DBP. The results suggest that testicular atrophy caused by DBP is associated with an alteration in the activities of enzymes related with specific events of spermatogenesis.
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PMID:Testicular toxicity of di-n-butyl phthalate in adult rats: effect on marker enzymes of spermatogenesis. 236 10


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