Oxidative and antioxidative status in the testes of rats with acute epididymitis.

INTRODUCTION: Epididymitis is an inflammation or infection of the epididymis, a convoluted duct that lies on the posterior surface of the testicle. Oxidative stress due to excessive production of reactive oxygen species in epididymitis, impaired antioxidant defense mechanisms, or both, precipitates a range of pathologies that are currently believed to negatively affect the male reproductive function. How oxidative stress affects the testes is still unknown. We aimed to investigate the oxidative and antioxidative status of testes of rats with unilateral acute Escherichia coli epididymitis. METHODS: The study included 36 male Wistar albino rats which were divided into three groups. In the epididymitis group (n = 12), an E. coli suspension was injected into the right ductus deferens of rats, and the same amount of saline was injected in the saline groups (n = 12). No surgery was performed in the control group (n = 12) for baseline values. Rats were sacrificed after 24 h and the epididymis and testes removed. The infection was confirmed by histopathologic evaluation and microbiological tests. The oxidative status of testes was evaluated by measuring myeloperoxidase (MPO) activity, and antioxidative status was evaluated by measuring total antioxidant response (TAR) and total antioxidant capacity levels (TAC). RESULTS: MPO activity in both the ipsilateral and contralateral testes of the epididymitis group was significantly higher than those of the saline and control groups (p < 0.05). The TAR and TAC levels in both testes were also significantly elevated in the epididymitis group versus the two other groups (p < 0.05). CONCLUSIONS: Acute epididymitis causes an increase of oxidative stress in the ipsilateral and contralateral testes, but this condition is strived for to tolerate the increase of endogenous antioxidants.

Dietary magnesium depletion does not promote oxidative stress but targets apical cells within the mouse caput epididymidis.

It is well documented that a dietary deficiency in magnesium can induce oxidative stress and an inflammatory response in animal models. In our study, we have investigated these responses in the mouse epididymis after mice had been fed a magnesium-deficient diet for a 2-week duration. The extracellular and intracellular concentrations of magnesium where shown to be depleted on this diet. This was followed, however, only in the liver of the Mg-deficient animals, by an increase in both alpha 2-macroglobulin (alpha-2m), an acute phase marker, and interleukin-6 transcripts suggesting that an inflammatory response had been initiated. These changes were correlated with a decrease in circulating neutrophils. To address the question of whether or not peroxidation was induced in mouse epididymis following hypomagnesia, we have monitored the level of endogenous peroxidation, their ability to respond to induced peroxidation as well as the expression and activity of the enzymatic glutathione peroxidase (GPX) antioxidant family. To evaluate if the epididymis had evolved specific protections against peroxidation, other organs such as the liver and the kidney were monitored in parallel. We detected no evidence for increased peroxidation in any of the mouse organs tested. However, GPX activity was found to be significantly lower in the liver and the kidney of Mg-deficient animals while it was unchanged in the epididymides of the same animals during the deficiency. Histological analysis of the epididymis showed no major difference in the overall cytological aspect of the organ. Segment 2 of the caput, however presented a significant increase in the number of apically located cells or blebbing cells. Immunohistochemical analysis proved that these cells were epididymal apical cells and not infiltrated leukocytes. These observations suggested that the mouse caput epididymidis segment 2 specifically responded to Mg deficiency via the apical cells. Finally, a comparative analysis of stress response genes was conducted in control and magnesium-deficient caput epididymidis samples. It brought forward some genes that might be involved in the peculiar response of the caput epithelium following hypomagnesia.

Protein carboxyl methylase in asthenospermia.

Protein carboxyl methylase (PCM) activity was measured in human spermatozoa of 16 normal fertile men and 26 men with various forms of asthenospermia. PCM activities were in the range 14-635 pmol/min per 10(9) sperm. Six men with idiopathic asthenospermia had low PCM activity but the defect of sperm motility was not severe (sperm motility 25-50%). One man with zero sperm motility and sparse mitochondria in the midpiece spiral had high PCM activity. Two men, one with idiopathic asthenospermia and the other with asthenospermia following vasoepididymostomy, also had high PCM activities. PCM activity did not correlate with motility or motility index but there was a correlation between PCM activity and the proportion of immature forms in semen. Thus, the relationship between PCM activity and low motility of sperm is not simple and other cells also contribute to overall seminal PCM activity.

[Cholinesterase activity of sperm from rams infected with Brucella ovis]. / Izsledvaniia vurkhu kholinesteraznata aktivnost na sperma ot kochove, zasegnati ot Brucella ovis.

Studied were the indices of cholinesterase activity of semen taken from 23 normal rams and 23 rams infected with Brucella ovis, the latter being positive by the complement-fixation test and showing a varying deterioration of the semen production. The results obtained were processed biometrically. Established were dependable differences. The cholinesterase activity of semen of brucellosis-affected rams proved four times higher than that of normal rams' semen: 39.45 +/- 5.49 microleter TO2 for 1 hour as against 174.15 +/- 9.97 microleter. A reverse correlation was established between the values of the cholinesterase activity, and the pH value and the percent of pathologic forms of spermatozoa.

Epididymis and seminal vesicle as sources of carnitine in human seminal fluid: the clinical significance of the carnitine concentration in human seminal fluid.

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.