An investigation of urinary creatine excretion as a potential marker for testicular damage.

1. This study assessed urinary creatine excretion as a marker for testicular atrophy. 2. Male rats received a single i.p. dose of 2-methoxyethanol at 0, 250 or 750 mg kg-1 and were sacrificed 2 d later. Urinary creatine and creatinine excretion were measured on days 0, 1 and 2. 3. Decreased testicular weights and histopathological assessment revealed dose-related testicular damage. 4. On day 1, at both doses of 2-methoxyethanol, urinary creatine levels increased and creatinine levels decreased, resulting in a dose-related increase in the creatine/creatinine ratio. On day 2, the creatine/creatinine ratio was elevated relative to controls, but was less marked than on day 1. 5. The study confirmed that creatine excretion is a potential marker for acute testicular damage.

Quantitative high resolution 1H NMR urinalysis studies on the biochemical effects of cadmium in the rat.

Quantitative changes in the urinary excretion patterns of low molecular weight compounds were followed for up to 30 days after dosing of adult Sprague-Dawley rats with single intraperitoneal injections of CdCl2 (6-24 mumol/kg), using high resolution 1H NMR multicomponent urinalysis. There was a marked reduction in the rate of urinary excretion of citrate, 2-oxoglutarate, and succinate within 4.5 hr of the administration of 24 mumol/kg Cd2+. This continued for up to 4 days after dosing in male rats and was consistent with a renal tubular acidosis, caused by inhibition of carbonic anhydrase. Histological examination of the kidneys showed no evidence of structural abnormalities at any Cd2+ dose level. Creatinine excretion was not affected by Cd2+ treatment at any dose level but hippurate excretion was significantly reduced. Severe testicular damage was noted within 24 hr of Cd2+ treatment at doses of greater than 9 mumol/kg and the degree of damage appeared to be correlated with the presence of large amounts of creatine (up to 20 mM) in the urine. Analysis of homogenates of healthy testicular material indicated the presence of high concentrations of free creatine. Cadmium-induced creatinuria appears to result from direct release of creatine from the necrotic cells of the seminiferous tubules and, hence, the measurement of creatine excretion rates may provide a useful noninvasive indicator of testicular necrosis. Because NMR is nonselective in terms of metabolite detection, this work has shed new light on the changes in urinary composition arising from Cd toxicity. As such, the technique is potentially very valuable in the search for new metabolic markers of toxicity and organ dysfunction.

Urinary creatine as a possible marker for testicular damage: studies with the testicular toxic compound 2-methoxyethanol.

A single dose of 500 mg/kg of 2-methoxyethanol given to male rats caused testicular damage, detected by histopathology, a significant reduction in relative testis weight, and a significant rise in urinary creatine, maximal at 48 h after dosing. Further studies showed that the reduction in relative testis weight and creatine excretion were dose related. Conversely, urinary creatinine showed a dose-related decrease at 24 h after dosing. In female rats dosed with 500 mg/kg of 2-methoxyethanol, there was no increase in urinary creatine or decrease in creatinine. These data suggest that urinary creatine may be a useful, noninvasive marker of testicular damage.

[Urinary excretion of testosterone and androstenedione in hypogonadism in men]. / Vydelenie s mochoi testosterona i androstendiona pri gipogonadizme u muzhchin.

The authors present the results of determination of the testosterone and androstendion excretion in the patients with various forms of hypogonadism and in healthy men. Testosterone excretion was decreased in the patients with hypogonadism, against the background of normal or increased androstendion excretion whereas the degree of deviations of the testosterone/androstendion ratio depended on the clinical variant of hypogonadism. Thus, retarded or decreased accumulation of the enzymes in the testes responsible for the change from the "child" to the "mature" type of steroid biosynthesis could serve as a mechanism of hypogonadism occurrence, which should be taken into consideration in the elaboration of the methods of syndrome therapy of this type of pathology.

[Excretion of testosterone in men with various forms of hypogonadism]. / Ekskretsiia testosterona u muzhchin s razlichnymi formami gipogonadizma

A reduction of testosterone excretion in men with hypogonadism is reported in literature; however, the clinical peculiarity of its individual forms are not considered in these works. This paper treats of testosterone excretion in 43 patients with various forms of hypogonadism, of this number in 36 before and after a single testosterone-propionate loading. There was seen a reduction of testosterone excretion in hypogonadism. Secondary hypogonadism coursed against the background of a more marked insufficiency of testosterone excretion than the primary one. In a number of hypogonadism cases testosterone excretion remained unchanged and their clinical signs were caused by an inadequate realization of the androgenic effect. In hypogonadism an increase of the urinary excretion following its administration did not always correspond to the dose of the administered hormone, which could serve as one of the pathogenetic mechanisms of development of the disease.

Gonadal effects of vasectomy and vasoligation.

During a 28-week study, vasectomy and vasoligation of immature male Wistar rats revealed that there was a significant decrease in urinary 17-ketosteroid in the vasectomized group at week 15; at week 28 there were significant decreases in the weights of the testes of the test groups, as compared to those receiving sham operations, with maximum alterations in the vasectomized rats. Small, soft discolored testes with cysts in the cauda epididymis and vas deferens regions occurred frequently in the test groups. The output of 17-ketosteroid in the urine and the findings in the testes indicate significant alterations in the morphology and function of the testes and suggest the need for caution and extensive investigations in man before recommending vasectomy as a simple, innocuous, "physiologic" means to ensure conception control.

Plasma and urinary luteinizing hormone levels in the diagnosis of endocrine disease.

The diagnostic value of measurements of plasma and urinary luteinizing hormone (LH) has been studied in 209 patients with endocrine disease. In 44 patients puberty was either delayed or had failed to occur. In those with chromosomal abnormalities the LH levels were often within the normal range, whereas those with a pituitary cause usually had low levels. In boys with delayed puberty plasma LH levels rose before physical changes occurred and had prognostic value. In patients with later gonadal failure, men with impotence or infertility, and women with secondary amenorrhoea LH assays proved of little value, although in one case a premature menopause was suspected and six patients with anorexia nervosa had low LH levels.Sixty patients with disorders of the hypothalamicpituitary area were studied. Levels of LH were measured and considered in relation to the other anterior pituitary hormones. Impairment of LH secretion was one of the first effects on hormone production of disease affecting this area, and this was, of course, most readily detected in postmenopausal women.The normal ranges of both plasma and urine LH are wide and there seems to be considerable day-to-day variation, especially of urinary output. Several samples should, therefore, be measured if therapeutic decisions are involved.