Plasma Acid Phosphatase Activity Research Articles

Innate-immune responses of tilapia (Oreochromis mossambicus) exposure to acute cold stress.

In this present study, Oreochromis mossambicus tilapia were transferred to cold water at 12°C for various time intervals (1, 4, 8, 24, and 48 hr) and its innate immune response was analyzed by studying cellular and humoral parameters. In vivo, alternative complement pathway activity in blood plasma was rapidly increased at 1 hr of cold water (12°C) exposure. Lysozyme activity and cortisol levels of plasma were increased at 4 and 1 hr, respectively. Surprisingly, only plasma cortisol levels remained unchanged through 24 hr of cold water transfer. Phagocytic ability, phagocytic capacity, and respiratory burst (RB) activity of head kidney (HK) leukocytes and splenocytes showed no any significant changes. In peripheral blood leukocytes, phagocytic capacity, and RB activity were increased at 24 hr of cold water exposure. The expressions of genes involved innate immunity in splenocytes and HK leukocytes of tilapia cold water exposure were analyzed, messenger RNA (mRNA) expressions of HSP70, HSP90, and immunoglobulin M failed to change upon exposure to cold stress. Major histocompatibility complex-I and II mRNAs were significantly increased in tilapia splenocytes at 1 hr of cold water transferred. Whereas myxovirus (Mx) expression was increased in splenocytes and HK leukocytes of tilapia after 1 hr of cold water exposed. Our result reveals that the exposure of tilapia to acute cold stress condition significantly enhances plasma acid phosphatase activity and both phagocytic capacity and RB activity. Furthermore, cold stress significantly stimulates Mx gene expression in splenocytes and HK leukocytes.

Effect of organic and inorganic forms of selenium in diets on turkey semen quality

The effects of Se supplementation and its organic or inorganic form on semen quantitative parameters (ejaculate volume, sperm concentration, and total number of sperm) and biochemical parameters of seminal plasma (protein concentration, acid phosphatase activity, superoxide dismutase activity, and total antioxidant capacity) were investigated over a 25-wk reproductive season. Additionally, DNA fragmentation and motility characteristics of turkey spermatozoa were measured. The parameters of turkey semen in relation to yellow semen syndrome were also determined. Twenty-four males (Big 6) were divided into 3 experimental groups differing in form of Se supplementation (no Se supplementation, 0.3 mg/kg of inorganic Se from sodium selenite and 0.3 mg/kg of organic Se from Sel-Plex, Alltech Inc., Nicholasville, KY). Dietary Se supplementation enhanced the sperm concentration and total number of sperm and did not influence the antioxidative properties of turkey seminal plasma and most biochemical parameters. Only seminal plasma acid phosphatase activity was increased in turkeys fed inorganic Se. The main sperm DNA fragmentation parameters were not affected by dietary Se. The highest percentage of motile spermatozoa (85%) was recorded for the semen of turkeys fed organic Se. Values of the biochemical parameters (acid phosphatase, superoxide dismutase, total antioxidant capacity) of seminal plasma increased during the reproductive season. Yellow semen was characterized by increased biochemical parameters and decreased spermatozoa motility characteristics. However, the percentage of motile spermatozoa did not differ between white and yellow semen. Organic Se seemed to be the preferred form of diet supplementation in comparison with inorganic Se. Biochemical parameters of semen and spermatozoa motility parameters appear to be useful for evaluating the effect of age on semen quality. Monitoring the DNA fragmentation of spermatozoa at the end of the reproductive season could be a useful tool for monitoring turkey semen quality. Increased superoxide dismutase activity can be used as an indicator of yellow semen. A decline in the quality of yellow semen can be related to a decrease in the spermatozoa motility parameters of turkeys.

The effects of dietary calcium during lactation on lead in bone mobilization: implications for toxicology.

Under a normal 1.0% calcium (Ca) concentration in the diet during and after chronic lead (Pb) intoxication, there was a significant increment in the concentration of Pb in the blood, kidney, liver and brain during lactation, parallel to a decrement of Pb in the bone. The increment of Pb in the brain was accompanied by an enhanced lipid oxidation (increase in conjugated dienes). During lactation, on the first 14 days, when dietary Ca was reduced to 0.05%, bone Ca concentration was decreased by 15%, bone resorption measured as acid phosphatase activity in plasma increased three times and Pb bone concentration dropped by 30%. Under a 0.05% Ca in the diet in the nonlactating rats, Ca in the bone decreases also, but there were neither increments in bone resorption nor Pb efflux from the bone. These results suggested that Pb efflux in the bone was related to bone resorption during lactation. Interestingly, when dietary Ca was enhanced to 2.5% in lactating rats, Ca concentration in the bone increased by 21%, but resorption did not decrease and Pb bone concentration decreased by 28%, enhancing toxicity. In the control Pb-exposed nonlactating rats under a 2.5% Ca in the diet, Ca concentration in the bone was increased (18%), and Pb concentration in the bone was unaltered. Since Ca metabolism changes drastically in humans during pregnancy and lactation, and it is likely that bone Pb is mobilized and transferred to the more available compartments of the maternal circulation, the increment in daily intake of Ca during lactation could enhance Pb efflux from the bone.

Acid phosphatase activity in hemolymph of the migratory grasshopper, Melanoplus sanguinipes, during Beauveria bassiana infection

AbstractThe distribution and abundance of acid phosphatase (AP) in hemolymph (HL), plasma (PM) and hemocyte lysate supernatant (HLS) of the migratory grasshopper, Melanoplus sanguinipes infected with Beauveria bassiana (strain GK 2016) has been examined. AP activity was determined at intervals from 30 min to 60 h postinjection of 2 μl of 1 times 108conidia/ml per grasshopper. The enzyme was detected with the substrate β‐glycerophosphate in sodium acetate acetic acid buffer form hemocytes (HC) and with p‐nitrophenol phosphate sodium salt for HL, PM and HLS. In results of experiment 1 proportion of HC showing AP activity increased 1–2 h, then returned to normal after 4 h. However, in B. bassiana‐injected grasshoppers, a second increase was noted 24 h later which was not seen in the Tween‐80‐injected insects. Uninjected controls showed no change with time in the proportion of HC with AP activity.Studies were also made of the distribution of AP activity in the HL, PM, and HLS. AP activity in HL appeared to vary with the sex of the grasshoppers. Females showed increase in AP activity in HL 18–24 h after injection with B. bassiana, whereas males only showed an increase 1 h after injection. Assay of HLS showed that the level of AP activity did not change significantly throughout the experiment. Changes in AP activity in PM, in both B. bassiana – and Tween‐80‐injected insects (both sexes) paralleled those of the HL, indicating that the enzyme is released from the HC. The observations are discussed in terms of the possible role of AP in the immune response of M. sanguinipes.

In vivo and in vitro studies of bacterial endotoxin-membrane interactions and the effects of membrane-active agents.

The characteristics of 51Cr-labelled E. coli endotoxin binding to human erythrocyte membranes in vitro have been investigated. A saturable component of binding was apparent at low endotoxin concentrations (less than 50 micrograms ml-1) relevant to its in vivo actions, while at higher concentrations binding was non-saturable and increased in linear fashion. Experiments examining the ability of unlabelled endotoxin to antagonize the binding of labelled toxin provided further evidence for these specific and non-specific modes of endotoxin-membrane interaction. Membrane-active agents previously shown to reduce endotoxin toxicity in vivo decreased endotoxin binding to erythrocyte membranes in vitro, with propranolol and pranolium being the most effective in this regard. Tissue distribution studies following administration of radiolabelled endotoxin to guinea-pigs showed a positive correlation between the accumulation of 51Cr-endotoxin in lung and elevations in plasma acid phosphatase activity, a measure of in vivo endotoxin toxicity. The in vivo accumulation of 51Cr-endotoxin in guinea-pig lung was reduced by prior treatment with (+)-propranolol or pranolium, paralleling the results of the in vitro binding studies. Our results suggest that membrane-active agents such as (+)-propranolol may be useful adjuncts to antimicrobial drugs in the therapy of gram-negative endotoxaemia.

Plasma acid phosphatase levels in endotoxaemia: modification by drugs and chemically detoxified endotoxins.

The ability of chemically detoxified E. coli endotoxins and membrane-active agents to modify the toxicity of native E. coli endotoxin in vivo was examined. The time- and dose-dependent increase in plasma acid phosphatase activity following toxin administration to rats provided a convenient quantitative measure of in vivo toxicity under various experimental conditions. Treatment of endotoxin with either sodium hydroxide or sodium periodate produced substances which, when injected alone, failed to cause an increase in plasma acid phosphatase activity. When given before native endotoxin, periodate-detoxified toxin produced a dose-dependent reduction in the elevation of plasma enzyme activity caused by unmodified toxin. Pretreatment with pranolium, hydrocortisone or (+)-propranolol also reduced the in vivo toxicity of endotoxin. Mortality studies in mice provided further independent support for the effectiveness of periodate-detoxified endotoxin and membrane-active drugs as endotoxin antagonists. Evidence has been found that under certain conditions gentamicin may act synergistically with bacterial endotoxins in vivo.

Delayed neurotoxicity from long-term low-level topical administration of leptophos to the comb of hens

The production of delayed neurotoxicity in hens following percutaneous administration of leptophos [ O-(4-bromo-2,5-dichlorophenyl) O-methyl phenylphosphonothioate] has been investigated. By applying a solution of the insecticide in acetone to the comb, seven groups of three laying hens were given daily a single percutaneous dose of 0.1, 0.5, 1.0, 2.5, 5.0, 10.0, or 20.0 mg/kg of leptophos for 183–323 days. All hens given 0.5–20 mg/kg developed ataxia. The group of hens given a daily dose of 0.1 mg/kg of leptophos showed no abnormalities in gait or behavior. The severity of the clinical condition depended on the size of the daily applied dose. The “latent period” and “total administered dose” before onset of ataxia depended on the daily topically applied dose. The most consistent histopathological changes were degeneration of myelin and axons in spinal cords of intoxicated birds. The severity of change was greatest in hens receiving the highest doses. While plasma cholinesterase was inhibited in all treated birds, plasma acid phosphatase activity was significantly increased. The present investigation shows that long-term low-dose applicaton of leptophos to the comb produced delayed neurotoxicity in hens similar to that reported for the oral administration of this compound.

Increased acid phosphatase activity in hens following an oral dose of leptophos

Oral administration of a dose of leptophos which does not produce delayed neurotoxicity to hens caused significant inhibition of plasma cholinesterase. The enzymatic activity which was lowest one half day after the administration gradually increased with time and was completely recovered on day 20. Plasma acid phosphatase activity significantly increased following the oral administration of leptophos, and the enzymatic activity was significantly higher than that of the control throughout the experiment. The increase in acid phosphatase activity is implicated in the mechanism of delayed neurotoxicity caused by leptophos in hens.

Amphibian acid phosphatase—II.: The effect of parathyroid extract on the lysosomal enzyme, acid phosphatase, in tissues of Rana pipiens

1. 1. Acid phosphatase activity is influenced by parathyroid hormone in amphibian skeletal tissues and plasma. 2. 2. The enzymatic response to parathormone is tissue-specific, varying in time, magnitude and direction of change. 3. 3. The diaphysis and epiphysis of the femur respond slowly to parathyroid extract treatment; at 1 hr after injection, acid phosphatase activities were little changed from control levels, but subsequently, a progressive increase was observed. Plasma enzyme activity rises through 4 hr. 4. 4. The metaphyseal plate of the femur and the spongy coracoid bone of the pectoral girdle respond rapidly and strongly to hormone treatment; from 1–4 hr after injection, their acid phosphatase activities are significantly elevated. 5. 5. Daily hormone treatment for 1 week elevates acid phosphatase activity in plasma and all skeletal tissues studied except femoral epiphysis. On day 8, enzyme activity of the latter had sharply declined. 6. 6. A significant hypercalcemia accompanies the enzymatic changes in skeletal tissues and plasma.

Plasma acid phosphatase in normal and pre-eclamptic pregnancy

Plasma acid phosphatase activity was measured in nonpregnant, normal pregnant, and severely pre-eclamptic women. The third trimester of pregnancy was associated with a rise in plasma acid phosphatase and severe pre-eclampsia with a marked rise in this enzyme. Possible sources of this elevation in acid phosphatase activity are the placenta, kidneys, pregnancy-associated plasma proteins, and blood platelets—with platelets the most likely.

Early radiation lethality: enzyme release and the protective action of soybean trypsin inhibitor.

SummarySoybean trypsin inhibitor (SBTI) can act to reduce early radiation lethality (<24 hours) in the 3-day chick as well as in the 14-day chick embryo. Plasma acid phosphatase activity was increased more than 2-fold in lethally irradiated chicks, but only small increases were demonstrated in groups that received near-lethal exposures or that were protected by SBTI before a lethal exposure.

Plasma acid phosphatase activity and bone dystrophies in the fowl

1. 1. Severe osteoclasis is seen in hens suffering from “cage layer osteoporosis” (which seems to have a familial background) or when a laying hen, susceptible to this condition, is fed on a diet containing only 1 per cent of calcium. In such hens the level of the plasma acid phosphatase activity becomes markedly raised. 2. 2. In immature normal fowls the activity of this enzyme fluctuates with age; no sex difference was observed. Birds of this age group, suffering from osteopetrosis, may show an increased acid phosphatase activity in their plasma. 3. 3. The possible connexion between osteoclastic activity and plasma acid phosphatase is discussed. Levels of plasma citrate and ultrafiltrable calcium were within the normal ranges in affected birds.