Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.2.1.36 (hyaluronidase)
 4,606 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Exposure to drinking water containing as much as 500 ppm aluminum chloride for periods of 30, 60, and 90 days had no apparent effect on male reproductive processes. In an attempt to correlate enzyme activity with particular spermatogenic cell types, postnatal development of testicular enzymes was studied. Eight enzymes were selected: hyaluronidase (H), lactate dehydrogenase isoenzyme-X (LDH-X), dehydrogenases of sorbitol (SDH), alpha-glycerophosphate (GPDH), glucose-6-phosphate (G6PDH), malate (MDH), glyceraldehyde-3-phosphate (G3PDH), and isocitrate (ICDH). Enzyme specific activities in testicular homogenates were determined. Two types of enzyme developmental patterns were observed. One was represented by H, LDH-X, SDH, and GPDH; and the other by G6PDH, MDH, G3PDH, and ICDH. The former was characterized by a change in enzyme activities from low in newborn to high in adult while in the latter this pattern was reversed. The two complementary enzyme systems crossed each other at puberty. Prior to puberty, only spermatogonial cells are present; sperm differentiation initiated at puberty adds spermatocytes and spermatids to the testicular cell population. Male rats were exposed to borax in their diet for periods of 30 and 60 days. Concentrations of boron were 0, 500, 1000, and 2000 ppm. At the end of each experimental period, the specific activities of the selected enzymes were determined in the testis and prostate. Correlations of enzyme activity with testicular histology and androgen activities of the male accessory organs were sought. In addition, plasma FSH, LH, and testosterone levels were measured to assess pituitary-testicular interaction. Plasma and testicular boron concentrations were determined and a minimum boron concentration which induced germinal aplasia and male infertility was estimated. In both 30 and 60 day feeding studies, male rats receiving 500 ppm failed to demonstrate any significant adverse effects. In contrast, male rats receiving 100 and 2000 ppm boron displayed a significant loss of germinal elements, although most of the Leydig and Sertoli cells appeared normal. Testicular atrophy was associated with a decrease in seminiferous tubular diameter and a marked reduction of spermatocytes and spermatogenic cells. These morphologic alterations were associated with a concomitant reduction of H, SDH, and LDH-X specific activities. In contrast, the specific activities of G3PDH and MDH were significantly elevated above control. The increase in these enzyme activities can be attributed to the relative enrichment of spermatogonial cells during the loss of spermatocytes and spermiogenic cells. Boron-induced male germinal aplasia was also associated with significantly elevated plasma FSH while plasma LH and testosterone levels were not significantly altered. Plasma testosterone levels were unaltered. Male fertility studies demonstrated that at the 500 ppm boron level, fertility was unaffected. However, at 1000 and 2000 ppm boron, male fertility was significantly reduced. Most effects were reversible within 5 weeks. However, the male group receiving 2000 ppm boron for 60 days remained sterile. There was no dose-related decrease in litter size or fetal death in utero. Therefore, the boron-induced infertility was apparently not due to a dominant lethal effect but rather to germinal aplasia. Boron appears toxic to spermatogenic cells at testicular concentrations of 6-8 ppm.
 ...
PMID:Assessment of environmental factors affecting male fertility. 44 58

Study of the activities of hyaluronidase, lactate dehydrogenase isoenzyme-X and the dehydrogenases of sorbitol, alpha-glycerophosphate, glucose-6-phosphate, malate, glyceraldehyde-3-phosphate and isocitrate in the testes of mice of different ages showed that the changes were correlated with the stages of spermatogenic cell differentiation. The first 4 enzymes had activities which were low in newborn mice and high in adults; this pattern was reversed for the other enzymes.
 ...
PMID:Developmental patterns of enzymes in mouse testis. 99 2

Single doses of procarbazine (MIH) were injected IP at 0, 50, 100, 200, and 400 mg/kg body weight to CD-1 male mice. Activities of hyaluronidase, lactate dehydrogenase isoenzyme-X, and the dehydrogenases of sorbitol, alpha-glycerophosphate, glucose-6-phosphate, malate, isocitrate, and glyceraldehyde-3-phosphate in the testes of the mice were determined and correlated with changes in spermatogenic cell types in seminiferous tubules. All enzyme activities were higher than controls or remained unchanged on days 10-20 after drug treatment. Activities of hyaluronidase, sorbitol dehydrogenase, and lactate dehydrogenase isoenzyme-X decreased significantly to below normal levels on day 30 after drug treatment for all doses, whereas those of the other five dehydrogenases remained significantly higher than controls. All enzyme activities approached control levels with the concomitant recovery of spermatogenesis by day 60 after drug treatment. Histological examination of seminiferous tubules revealed that premeiotic spermatocytes were significantly reduced on days 10-20 but reappeared on day 30 after MIH treatment (400 mg/kg). The postmeiotic spermatogenic cells were unaffected at the time of MIH treatment, but had disappeared completely on day 30 after drug treatment. MIH, at the highest dosage, selectively destroyed spermatogonia and premeiotic spermatocytes; however spermatozoa and elongated spermatides were unaffected. This study demonstrated that the cytotoxic effect of MIH on spermatogenesis could be evaluated via changes in testicular enzyme activities. The present studies demonstrated that hyaluronidase, sorbitol dehydrogenase, and lactate dehydrogenase isoenzyme-X could serve as useful biochemical markers for assessing testicular toxicity induced by drugs and chemicals.
 ...
PMID:Selected testicular enzymes as biochemical markers for procarbazine-induced testicular toxicity. 651