Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.1.3.1 (alkaline phosphatase)
47,916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Male albino rats were treated with depot medroxyprogesterone acetate (1 mg/animal/day) + testosterone ananthate (100 micrograms/100 g body weight/day) for 30 and 60 days. After 30 days of treatment, all the testicular enzymes like beta-glucuronidase, hyaluronidase, sorbitol dehydrogenase, lactate dehydrogenase, acid and alkaline phosphatase, registered non-significant decrease in their values. Fifty percent of the treated animals achieved sterility after 30 days of treatment. After 60 days of treatment the testis showed degenerative changes in Golgi phase and late spermatids. Changes in the Golgi phase spermatids were related with degeneration of the nuclear membrane. Changes in the late phase spermatids included mitochondrial hypertrophy of the midpieces, membrane lysis, absence of cristae and degeneration of annulus leading to detachment of tail. Cytoplasm of luminal area displayed hypertrophied mitochondria devoid of cristae, prominent appearance of Golgi bodies, intense lysosomal activity and ample vacuolation. Tail fragments of degenerated spermatids prevailed in luminal cytoplasm. Except for beta-glucuronidase which registered a significant decrease, levels of all the other testicular enzymes, viz. hyaluronidase, lactate dehydrogenase, sorbitol dehydrogenase, acid phosphatase and alkaline phosphatase were within their control limits. The ultrastructural and biochemical changes are correlated.
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PMID:Effect of depot medroxyprogesterone acetate and testosterone ananthate on the testis of albino rats: ultrastructural and biochemical studies. 129 76

We sought to determine if there were any differences in the results of clinical laboratory tests between blood samples collected from the orbital venous plexus and the posterior vena cava of adult male rats. Thirty healthy adult male Sprague Dawley rats were anesthetized by ether inhalation, and blood samples were collected successively from the orbital venous plexus (OVP) and the posterior vena cava (PVC) for hematologic (n = 10), serum chemistry (n = 10), and coagulation (n = 10) analyses. The prothrombin and partial thromboplastin times of samples from the OVP were prolonged (17% and 288%, respectively) when compared with samples from the PVC. Respective hematologic biases were as follows: red blood cell count (7%), hemoglobin (6%), hematocrit (5%), mean corpuscular volume (-3%), mean corpuscular hemoglobin (-1%), mean corpuscular hemoglobin content (1%), white blood cell count (13%), and platelet count (-7%). Respective serum chemistry biases were as follows: sorbitol dehydrogenase (-7%), glucose (-7%), blood urea nitrogen (-10%), creatinine (-2%), total protein (4%), albumin (2%), globulin (9%), alkaline phosphatase (5%), lactate dehydrogenase (-6%), aspartate aminotransferase (-5%), alanine aminotransferase (-2%), total bilirubin (0%), direct bilirubin (0%), magnesium (-17%), sodium (4%), potassium (0), chloride (4%), calcium (-2%), phosphorous (-17%), cholesterol (3%), triglycerides (24%), creatinine kinase (-8%), 5'nucleotidase (0%), and total bile acids (4%). For hematologic testing, there were no biologically significant differences between samples collected from the OVP and PVC. The coagulation times and serum Mg and P showed biologically significant differences between samples collected from the OVP and PVC.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of bleeding site on clinical laboratory testing of rats: orbital venous plexus versus posterior vena cava. 132 Jan 64

1. Blood characteristics of reindeer calves fed on lichens were studied during the winter. 2. The serum total protein, albumin and globulin concentrations decreased during the winter, obviously partly due to protein deficiency in the diet. 3. High urea levels in autumn and midwinter were possibly reflections of increased stress and/or protein catabolism. 4. Marked lipolysis occurred in late winter, and thus increases were observed in fatty acids, glycerol, triglycerides and acetoacetate concentrations. 5. Serum sorbitol dehydrogenase (SDH) activity increased towards the spring, most probably reflecting changes in the liver. 6. A decrease in serum alkaline phosphatase (AP) activity occurred in midwinter due to cessation of growth. 7. It can be concluded that all the animals were at least in moderate condition throughout the winter and the physiological responses to a negative energy balanced reflected good adaptation.
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PMID:Blood chemistry of reindeer calves (Rangifer tarandus) during the winter season. 135 15

The purpose of this study was to determine the chronic toxicity of methidathion, an organophosphate insecticide, in dogs. Groups of beagle dogs, four/sex/dose, were fed methidathion at constant dietary concentrations of 0, 0.5, 2, 4, 40, or 140 ppm for 1 year. The equivalent daily dosages were approximately 0, 0.02, 0.07, 0.15, 1.4, and 4.7 mg/kg. There were no deaths or adverse clinical signs associated with the treatment. Weekly body weights and weight gains were not affected. Mean daily food consumption was reduced in male dogs given the 140-ppm diet. Major treatment-related effects were cholestasis, chronic inflammation in the liver, and cholinesterase (ChE) inhibition. The liver effects were indicated by gross and microscopic pathologic findings as well as moderate increases in serum bile acids and enzyme activities (alanine aminotransferase, aspartate aminotransferase, sorbitol dehydrogenase, and alkaline phosphatase) in all dogs receiving greater than or equal to 40 ppm. RBC ChE was inhibited in males at greater than or equal to 40 ppm and in females and 140 ppm. Brain ChE was inhibited in both sexes at 140 ppm; the magnitude of inhibition relative to control was slightly greater with the cerebellar fraction than with the cerebral fraction. Serum ChE was not affected at any dose level. In conclusion, liver was the target organ in beagle dogs given greater than or equal to 40 ppm (equivalent to 1.4 mg/kg/day) methidathion in diet for 1 year. The no-observable-effect level was 4 ppm (0.15 mg/kg/day) for both liver cholestasis and ChE inhibition.
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PMID:One-year dietary toxicity study with methidathion in beagle dogs. 151 89

The susceptibility to lipid peroxidation (LPO) of liver, kidneys, brains, lungs, heart, and testes was assessed in rats administered intraperitoneally with various doses of cadmium (Cd). Dose-response studies were carried out with male Long Evans rats (12-week-old; 300 +/- 33 g) injected with 25, 125, 500, and 1250 micrograms Cd/kg as CdCl2 and sacrificed after 24 h. In time-response studies, animals were administered with 25 and 500 micrograms Cd/kg as CdCl2 and sacrificed after 2, 6, 12, 24, and 72 h. Exposure of rats to low and moderate doses of Cd by the intraperitoneal route stimulated LPO in all the tissues investigated as assessed by the measurement of thiobarbituric acid reactive substances (TBARS). Lungs and brain were the most responsive, and these tissues and liver displayed early responses following Cd exposure. Comparison of LPO to various tissue indicators (for liver: alanine aminotransferase (ALT), sorbitol dehydrogenase (SDH), alkaline phosphatase (ALP); for lungs: ALP, gamma-glutamyl transpeptidase (GGT] suggested that low doses of Cd stimulated LPO without any evidence of acute damages. These results suggest that LPO is an early and sensitive consequence of Cd exposure as determined in various organs. Investigation of liver, lungs, and heart antioxidant defense system components (glutathione peroxidase (GPX), glutathione reductase (GR), glucose-6-phosphate dehydrogenase (G6PDH), superoxide dismutase (SOD] revealed that GPX might be considered as a potential modulator of the Cd-induced LPO reaction in lungs and heart tissues.
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PMID:Studies on lipid peroxidation in rat tissues following administration of low and moderate doses of cadmium chloride. 182 34

Testis of male albino rats treated with depot medroxyprogesterone acetate DMPA, at the dose of 1 mg/animal/day for 60 days showed degenerative changes in the late spermatids. The changes were related with the mitochondrial sheath of the midpiece, including the plasma membrane enclosing the mitochondria and the mitochondrial cristae. Except lactate dehydrogenase and alkaline phosphatase, all the testicular marker enzymes, viz. beta-glucuronidase, hyaluronidase, sorbitol dehydrogenase and acid phosphatase registered a significant decrease. The ultrastructural and biochemical changes are correlated, as the cellular degeneration is responsible for decrease in the activity of the marker enzymes.
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PMID:Effect of depot medroxyprogesterone acetate on testis of albino rats: ultrastructural and biochemical studies. 183 39

2-Mercaptobenzimidazole (2-MBI), used in rubber processing, is a suspect carcinogen structurally related to ethylene thiourea. The inhalation toxicity of 2-MBI was evaluated in male and female F344/N rats exposed 6 hr/day, 5 days/week to respirable aerosols generated by spray atomization of aqueous suspensions of the 2-MBI powder and subsequent drying of the resulting aerosols. Twelve exposures at target concentrations of 0, 6.3, 12.5, 25.0, 50.0, or 100 mg/m3 of 2-MBI produced a dose-related reduction in body weight gains, thyroid follicular cell hyperplasia, adrenal cortex fatty change, and pituitary atrophy. Sub-chronic exposures were conducted at target concentrations of 0, 3.1, 6.2, 12.5, 25.0, and 50.0 mg/m3 of 2-MBI. Rats at greater than or equal to 25 mg/m3 displayed hunched posture, hypoactivity, and reduced body weight gain, with compound related mortality at the highest exposure level. Anemia; increased SGPT, SGOT, alkaline phosphatase, sorbitol dehydrogenase, BUN, and cholesterol; and reduced free fatty acid were seen in rats at greater than or equal to 25 mg/m3. Increased thyroid weight and thyroid follicular cell hyperplasia were noted in both sexes at greater than or equal to 6.2 mg/m3, with reduced triiodothyronine and thyroxine levels in both sexes at greater than or equal to 12.5 mg/m3. Thyroid follicular cell hyperplasia was also seen in rats at 3.1 mg/m3. Thymus weights were significantly reduced in both sexes at all exposure levels with liver weight increases at greater than or equal to 6.2 mg/m3. Exposure-related histopathologic changes included pituitary cytoplasmic vacuolization, adrenal cortex necrosis, lymphoid depletion, thymic atrophy, liver cell hypertrophy, renal mineralization and tubular atrophy, and hypocellularity of the bone marrow.
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PMID:Prechronic inhalation toxicity studies of 2-mercaptobenzimidazole (2-MBI) in F344/N rats. 201 41

Rats were treated with trichloroethylene via intraperitoneal (ip) injection or inhalation, or with ip alpha-naphthylisothiocyanate (ANIT). Serum samples were assayed for indices of liver injury including alanine aminotransferase (ALT), sorbitol dehydrogenase (SDH), alkaline phosphatase (AP), and bilirubin. Liver from some rats was examined for histological appearance. These data were compared to levels of individual serum bile acids (SBA) determined by high-performance liquid chromatography. Trichloroethylene and ANIT, each at their highest dose only, caused elevations in ALT, but not SDH or AP. The highest dose of ANIT also caused elevated serum bilirubin and cholangitis in the liver. SBA were also elevated in response to both trichloroethylene and ANIT, but at doses below those at which other parameters of liver function were increased. For both chemicals, taurocholic acid was the most sensitive of the bile acids assayed, being elevated at the lowest doses tested of 10 mumols/kg for trichloroethylene and 5 mumols/kg for ANIT. As the doses were raised more of the individual bile acids showed increases. On exposure to trichloroethylene via inhalation taurocholic acid was one of two SBA to show elevation. Thus, both trichloroethylene and ANIT cause elevation in SBA at doses well below those which cause an increase in standard indicators of liver dysfunction. This suggests that SBA and perhaps taurocholic acid, in particular, may provide a sensitive tool for studying hepatobiliary effects of chemicals.
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PMID:Elevation of individual serum bile acids on exposure to trichloroethylene or alpha-naphthylisothiocyanate. 221 16

In a five-week feeding trial, 90 broiler chicks were used to study the response of serum and liver alanine aminotransferase (ALT) aspartate aminotransferase (AST), sorbitol dehydrogenase (SDH) and alkaline phosphatase following the replacement of varying levels (0, 20, 40, 60, 80 and 100 per cent) of fishmeal protein by soyabean meal protein. The results showed that both serum ALT and AST activities increased significantly (P less than 0.01) with the increasing levels of substitution of soyabean meal for fishmeal. Regression analysis showed a significant (P less than 0.01) positive correlation between ALT and AST activities and the level of soyabean meal substitution with correlation coefficient, r, of 0.93 and 0.98, respectively. The liver ALT and AST tended to increase with the increasing proportion of soyabean meal although such increases were not significant (P greater than 0.01). Serum and liver SDH and alkaline phosphatase activities were not significantly influenced by diet.
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PMID:Dietary fishmeal versus soyabean meal: an assessment of serum and liver enzyme response in the chicken. 235 76

A single oral dose of di-n-butyl phthalate (DBP) to male rats caused histologically a sloughing of the germ cells at 6 h. On Days 1 and 2 more severe sloughing was seen, followed by atrophy and the dissociation of the germ cells from the Sertoli cells and the spermatogonia. Biochemically, there was elevation of gamma-glutamyl transferase, a decrease in sorbitol levels at 3 h and a decrease in the activity of aldose reductase at 6 h, in the testes of treated rats. This was followed by decreases in fructose levels and increases in the activity of lactate dehydrogenase (LDH) and in lactate levels at 12 h, and decreases in the activities of sorbitol dehydrogenase and succinate dehydrogenase on Day 2. LDH isoenzymes 4 and 5 increased at 6 h prior to the increase in lactate levels. Increases in the levels of inositol and the activities of alkaline phosphatase and lactate dehydrogenase were also observed. Thus, these data suggest that DBP-induced testicular toxicity is caused by a shortage of energy fuels from glucose metabolism or by an anoxia.
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PMID:Mechanism of testicular atrophy induced by di-n-butyl phthalate in rats. Part 2. The effects on some testicular enzymes. 239 8


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