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)

After i.m. injection of [3H]butyrobetaine into rats, the accumulation of carnitine into the epididymis, prostate gland, seminal vesicles, testis and heart was studied. The concentration of radiolabeled carnitine into the cauda epididymis increased linearly with time up to 72 h after the injection of the precursor, while its level in the prostate and seminal vesicles decreased rapidly. Very low levels of carnitine were found in the testis. Castration reduced the carnitine accumulation by cauda epididymis to 6% of the control levels while treatment of castrated animals with testosterone propionate (500 mug/day) partly restored the carnitine uptake. Similar treatment with 17beta-oestradiol valerate or 17alpha-hydroxyprogesterone had no effect. Surprisingly, cyproterone acetate (5 mg/day) also significantly stimulated carnitine accumulation by the epididymis to a level above that of the castrated controls. Simultaneous injection of both cyproterone acetate and testosterone propionate to castrated animals caused an additive effect of these steroids. This indicated that cyproterone acetate in this system is working as a weak androgen. Treatment of rats with 17beta-oestradiol valerate also reduced carnitine accumulation by the cauda epididymis. This is due to suppression of pituiatry gonadotrophin secretion, since concommitant treatment with testosterone propionate (500 mug/day) caused a normalization of the carnitine uptake. Treatment of intact rats with cyproterone acetate significantly reduced the epididymal weight, but not the carnitine accumulation. 17alpha-Hydroxyprogesterone treatment had no effect either on the epididymal weight or the accumulation of the carnitine. Unilateral orchiectomy reduced the carnitine accumulation by the cauda epididymis to about 40% of that occurring in the non-operated control side. This indicates that the luminal contact between the testis and epididymis or the luminal content of the epididymis itself is of importance for the androgen-dependent metabolic process occurring in the cauda epididymis. Castration or hormone treatment did not change the conversion of butyrobetaine to carnitine, or the carnitine uptake by heart. Carnitine uptake by the testis after [3H]butyrobetaine injection was rather low and this would exclude the possibility of synthesis of carnitine in the testis as a source of epididymal carnitine. Carnitine only accumulated in the cauda epididymis in vivo 4 to 96 h after injection of [3H]butyrobetaine. The presence of radioactively labeled butyrobetaine or methylcholine was not detected.
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PMID:Androgen-dependent accumulation of carnitine by rat epididymis after injection of [3H]butyrobetaine in vivo. 17 Jan 50

Luminal fluid was collected by micropuncture techniques from the testis and epididymis of the rat, hamster, rabbit, boar and ram and the concentration of free L-carnitine in the fluid was estimated using enzymic methods. Carnitine was present in the testicular fluid of the rat in concentrations less than 1 mM but increased down the epididymis to reach 53 mM in luminal fluid from the cauda epididymidis, approximately 2000 times higher than in blood plasma. A high concentration was first found in the luminal fluid from the distal caput epididymidis, at about the point where the spermatozoa become motile. Carnitine was also present in the epididymal luminal fluid of the other species studied; the amounts were not as high as those in the rat but were still higher than those in blood plasma.
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PMID:The concentration of carnitine in the luminal fluid of the testis and epididymis of the rat and some other mammals. 46 29

After i.m. injection of [3H]butyrobetaine into intact and castrated rats, the specific activity of plasma carnitine remained nearly constant over 24--96 h and epididymal uptake of carnitine was constant per unit time up to 72 h. The uptake ratio of intact to castrated rats was high at 48, 72 and 96 h after injection. Administration of estradiol valerate over 20 days reduced carnitine uptake in epididymis. This reduction was dose-dependent when estrogen was administered i.m. at 0.33--10 microgram/day levels. A maximum reduction of 90% was obtained with the 10 microgram dose. A dose increase from 33 to 100 microgram/day caused no further reduction. Norspiroxenone (2--10 mg/day) and SK 7670 (1.5 and 7.5 mg/day) were less effective than estradiol valerate (10 microgram/day) in suppressing carnitine uptake in epididymis. Epididymal carnitine uptake in estradiol valerate treated rats (33 microgram/day for 20 days) increased in a time- and dose-dependent manner under testosterone propionate treatment (50, 250, 1250 microgram/day). Carnitine uptake increased to 80% of the nonsuppressed levels when testosterone propionate was adminsitered over a 6-day period at 1250 microgram/day. Dihydrotestosterone increased epididymal carnitine uptake to the same extent as testosterone propionate. delta4-androstene-3,17-dione and 5alpha-androstane-3alpha,17beta-diol (50 microgram/day) were less effective, stimulating uptake to only 15% and 40% respectively of the testosterone propionate (250 microgram/day) stimulated levels. Changes in epididymal carnitine uptake evoked by various experimental procedures were closely paralleled by weight changes in the ventral prostate. This response resemblance indicates a similarity between the androgen sensitivity of the prostate gland and that of the carnitine uptake system in epididymis. The dose-dependent effect of estrogen on the accumulation of epididymal carnitine, together with the marked responses induced in this system by manipulation of its androgen status, support a possible use for the system as an assay for androgen or antiandrogen potency in vivo.
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PMID:Accumulation of carnitine in rat epididymis after injection of [3H]butyrobetaine in vivo: quantitative aspects, and the effects of androgens and antiandrogens. 68 Mar 41

Diabetes, starvation and various hormonal treatments are known to alter drastically carnitine concentrations in the body. Before the mechanisms controlling carnitine metabolism could be determined, it was necessary to establish normal carnitine concentrations in both sexes at different ages. Carnitine was assayed in plasma, liver, heart and skeletal muscle of rats from birth to weaning. The plasma carnitine increased rapidly during the first 2 days after birth. Carnitine in both heart and skeletal muscle increased, whereas liver concentrations declined during the first week of life. A carnitine-free diet containing sufficient precursors for carnitine biosynthesis was fed to weanling rats. Groups of ten male and ten female rats were killed each week for 10 consecutive weeks. Carnitine was determined in plasma, liver, heart, skeletal muscle, urine and epididymis in the male. There was no difference in carnitine concentrations between the sexes at weaning. Plasma, heart and muscle concentrations were higher in adult male rats than in adult females. However, liver carnitine and urinary carnitine concentrations were higher in adult female than in adult male rats. The epididymal carnitine concentration increased very rapidly during 50 to 70 days of age and the differences in carnitine concentrations between the sexes also became apparent during this time. Thus both the age and the sex of the human subject or experimental animal must be considered when investigating carnitine metabolism.
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PMID:Variation in tissue carnitine concentrations with age and sex in the rat. 74 45

Carnitine determinations in human seminal fluid were shown to be useful in assessing epididymal and seminal vesicle function and in locating blockages in the male reproductive tract. The carnitine concentrations in 50 samples of seminal fluid ranged from 15 to 530 mug/ml (as carnitine-HCl). The patients could be divided into four classes. Patients with normal seminal vesicle and epididymal function had values of 250 mug/ml or above. Those with a defective epididymis and a functional seminal vesicle had intermediate carnitine levels (100 to 200 mug/ml) and normal fructose values in the seminal fluid. Patients with a defective seminal vesicle but a functional epididymis had intermediate carnitine concentrations and low fructose levels. Extremely low carnitine values (less than 100 mug/ml) were found in seminal fluid from patients whose epididymis and seminal vesicle both were defective. The possible role of carnitine in sperm maturation was discussed.
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PMID:Epididymis and seminal vesicle as sources of carnitine in human seminal fluid: the clinical significance of the carnitine concentration in human seminal fluid. 124 48

15 subjects with Hypogonadotropic Hypogonadism (HH) were treated with either gonadotropins (13 cases) or pulsatile subcutaneous Luteinizing Hormone Releasing Hormone (LHRH) (2 cases) for up to 42 months, to study the effects of therapy step by step. The following results were obtained: (A) In postpubertal HH (5 cases = Group A), therapy brought about onset of spermatogenesis within 3 months and its normalization within 6 months. In HH of prepubertal onset (10 cases = Group B), spermatogenesis started within 9 to 21 months and became normal in only 3 cases after at least 18 months. The best sperm counts were obtained in Group A in the third month of treatment (41.75 +/- 43.68 mil./ml) and in Group B in the 36th month (14.87 +/- 17.06 mil./ml). Sperm motility was normal in the majority of the cases in Group A from the beginning but did not become normal in Group B. (B) Seminal fructose and zinc were normal from the beginning of therapy in 66% of the cases in both groups. Zinc became normal in 100% within 3 months in Group A, in Group B within 18. Carnitine was normal in 50% of cases in both groups, contemporaneous with sperm appearance. Transferrin was normal in Group A after appearance of spermatozoa, but in Group B never became normal. (C) We hypothesize that the recovery of fertility passes through the following stages: (1) Functional recovery of Leydig cells, followed by seminal vesicles and prostate. (2) Recovery of epididymal function, which probably implies beginning of the tubular function. Recovery of Sertoli cell function occurs with more difficulty.
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PMID:Achievement of spermatogenesis and genital tract maturation in hypogonadotropic hypogonadic subjects during long term treatment with gonadotropins or LHRH. 177 42

Carnitine is present in seminal fluid either as a free compound or in acetylated form, and as can be inferred from the latest studies, it is of epididymal origin. In the present study, a comparative analysis has been made between carnitine levels in a group of subjects made up of fertile males and another group composed of patients with varying degrees of oligo-asthenospermia. The levels of free carnitine were measured through the enzyme-colorimetry method of Marquis and Fritz. It was found that carnitine levels were significantly lower in the oligo-asthenospermic group, and that such levels decreased progressively as the degree of oligo-asthenospermia increased. On the other hand, a regression analysis showed an increase in carnitine values as seminogram parameters measuring sperm motility and maturation (vitality, active motility, hypo-osmotic test, sperm count per ml and total sperm count of ejaculate) increased. Such differences lead us to think that carnitine plays an important role in the maturation process and in development of sperm motility.
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PMID:[Evaluation of seminal carnitine as a marker of epididymal function]. 276 83

In a previous study we showed that the administration of gossypol to rats for 34 days caused 2 types of modification of the epididymis: (1) the secretion of carnitine and inositol were reduced in the fluid, (2) the spermatozoa lost their motility and showed major morphological changes (head-flagella dissociation). We wished to clarify the early effects of gossypol on the epididymis. Sprague Dawley adult rats (350 g) were forced fed with gossypol at a dose of 25 mg/kg/day for 17 days. After sacrifice, the motility of spermatozoa from the cauda of the epididymis was measured and the morphology of spermatozoa from the caput of the epididymis quantified following electron microscopic examination. Carnitine, inositol and potassium were assayed in the epididymal fluid. No abnormalities of spermatozoa (motility, count, morphology, ultrastructural examination) were observed in the cauda of the epididymis. In contrast, a high percentage (63%) of spermatozoa from the caput of the epididymis were altered (vacuolization and lysis of mitochondria). Biochemical analysis of the fluid revealed no differences between treated animals and controls. Thus it appeared therefore, that after 17 days of gossypol administration, the only abnormality detected in the epididymis involved the spermatozoa from the caput. It is therefore probable that the motility disorders seen in spermatozoa from the cauda of the epididymis at 34 days cannot be explained by alterations of the secretion of fluid but rather by earlier direct lesions of testicular spermatids and/or of spermatozoa from the caput of the epididymis.
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PMID:Early effects of gossypol on the testis and epididymis in the rat. 325 3

Carnitine and its short-chain acyl esters were assayed in semen from normospermic and azoospermic men. Extremely low concentrations of free carnitine and acylcarnitine were found in semen from patients with obstructive azoospermia where the ejaculate was primarily of prostatis origin, and low values were also obtained in obstruction of the vas deferens, where the epididymal contents were not ejaculated. Semen from patients whose azoospermia was caused by testicular dysfunction had low acylcarnitine concentrations and normal levels of free carnitine in most cases, but a group of patients with severe testicular failure (including cases of Klinefelter syndrome and cryptorchidism) had low semen free carnitine concentrations. Whereas treatment with human chorionic gonadotropin increased serum testosterone levels in azoospermic patients, it did not increase the free carnitine concentration in semen, although it increased the proportion of carnitine found in acylcarnitines.
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PMID:Carnitine and acylcarnitines in semen from azoospermic patients. 611 78

1. L-carnitine and its short-chain acyl derivatives were measured in semen of boar, man, rooster, bull, squirrel monkey and ram. 2. Carnitine was present in concentrations of 220, 476, 540, 1880, 3330 and 3820 muM respectively, and acetylcarnitine concentrations were 2, 191, 354, 709, 259 and 2750 muM. Propionyl and C4-acyl carnitines were found in small quantities. 3. Analysis of sequential "Split-ejaculate" samples of boar semen showed that carnitine concentration correlated with sperm count, suggesting an epididymal origin for this substance in this species. 4. Bioautographic analysis of samples obtained from ram and rat indicated that carnitine and acetylcarnitine were present in epididymal fluid and in fluids from accessory glands of the male reproductive tract.
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PMID:A comparative study of carnitine and acylcarnitine concentration in semen and male reproductive tract fluids. 712 5


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