Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.6.1.3 (ATPase)
 65,361 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Zinc deficiency (ZD) is teratogenic in rats, and fetal skeletal defects are prominent. To elucidate further the effects of maternal ZD in the fetal skeleton, we performed a morphological and histochemical study of tibial growth plate (GP) in ZD rat fetuses. The histochemical study included the identification of calcium, of hydrolytic enzymes associated with the process of calcification, and of oxidative enzymes related to energy production and to the synthesis of proteoglycans. Pregnant Sprague-Dawley rats were fed (1) a control diet (76.4 micrograms Zn/g diet) ad libitum (group C), (2) a zinc-deficient diet (0 micrograms/g) ad libitum (group ZD), or (3) the control diet pair-fed to the ZD rats (group PF). On day 21 of gestation, laparotomies were performed, the fetuses were removed, and fetal tibiae obtained. Specimens were stained with hematoxylin-eosin (H&E) and Masson Trichrome and were processed for identification of alkaline phosphatase, adenosine triphosphatase, succinic dehydrogenase, NADH dehydrogenase, and calcium. The morphologic patterns found in ZD fetal tibiae indicated defects in various cell types implicated in bone metabolism. Staining for hydrolytic enzymes revealed alterations in the size and distribution of matrix vesicles and a weaker staining for ATPase in ZD fetuses. Staining for oxidative enzymes was overall more intense in ZD fetal tibiae. ZD fetuses also presented irregular and defective calcification. These findings indicate that severe maternal ZD in the rat results in structural and functional alterations in the GP of fetal bone, leading to a defective endochondral ossification.
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PMID:Changes in the fetal tibial growth plate secondary to maternal zinc deficiency in the rat: a histological and histochemical study. 196 89

Zinc, protein, cholesterol, phospholipids, alkaline phosphatase (AlPase), acid phosphatase (AcPase), adenosine-5-triphosphatase(ATPase) and histology were studied in testis of zinc-deficient mice. Zinc and protein decreased in the 3-week experiment whereas they increased in the 6-week experiment. Zinc is involved in several functions of the cell and is regulated by hormones. Inhibition of spermatogenesis indicates for decreased zinc levels in 3-week whereas the increase in 6-week experiment indicates for accumulation of zinc in oedomatous fluid and uncontrolled diffusion of zinc across the blood testis barrier. Glycogen decreased in the 3-week as well as 6-week experiments due to blockage of androgen and spermatogenesis. Cholesterol and phospholipids increased in the 3-week experiment and decreased in 6-week experiment as both the parameters are related to steroidogenesis. Zinc deficiency leads to aspermatogenic condition and comparatively less injury to non-germinal cells. This could have blocked the transport of material across the testis barrier and therefore might have increased AlPase levels. Increased AcPase, probably represents lysosomal enzymes, as the cell debris of disorganised epithelium are to be digested and removed. ATPase increased in 3-week experiment and can be correlated to increased demands of energy of testicular cells to overcome the insults of zinc deficiency whereas the decrease in 6-week experiment could be as a result of inhibition of spermatogenesis.
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PMID:Histological and biochemical changes in testis of zinc deficient BALB/c strain of mice. 808 79

The effects of zinc on growing rats were characterized using the dietary zinc-deficient (ZD) and Zinc-overdose (ZO) models. Zinc deficiency had negative effects on the host final body weight and liver zinc content, whereas zinc overdose had positive effects. In order to identify the molecular changes in the liver responding to dietary zinc status, cDNA microarrays were used to analyze the expression pattern of 9753 genes in the livers of rats fed ZD and ZO diet for 6 wk, compared with zinc-adequate ZA. The mRNA levels for 62 genes were affected significantly by the ZD diet, whereas 66 gene transcriptions were markedly changed in the ZO diet. Those predominant gene products involved in nitrogen metabolism (glutaminase), carbohydrate metabolism (aldolase), lipid metabolism (stearoyl-CoA desaturase), growth (insulin-like growth factor-binding protein), transcription and translation (zinc-finger protein), immune (natural-killer cell), signal transduction (mitogen- activated protein kinase), and ion transportation (ATPase Na+/K+ transporting peptide) were clustered. In conclusion, a number of mammalian genes related to zinc in the liver were identified. The characterization of the genes and their products will allow a more comprehensive analysis of the role of zinc in metabolism. Furthermore, the mRNA identified could be useful in establishing the mechanisms of zinc in the pleiotropic metabolisms in vivo.
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PMID:Gene expression profiles analysis of the growing rat liver in response to different zinc status by cDNA microarray analysis. 1743 60