Liver Alkaline Phosphatase Activity Research Articles

Metabolic and thyroidal response in air-breathing perch ( Anabas testudineus) to water-borne kerosene

To address the physiological compensatory adaptations in air-breathing fish to a toxicant, we studied the metabolite pattern, serum and liver enzymes and thyroidal response in a tropical air-breathing perch, Anabas testudineus (kept at 30 °C in a 12-h L:D cycle) after exposing the fish for 48 h to the water-soluble fraction of kerosene. The concentrations of serum glucose ( P < 0.05), triglycerides ( P < 0.01) and liver total protein ( P < 0.05) were significantly increased in kerosene-exposed fish. The serum urea level, however, remained unaffected. A significant ( P < 0.05) increase in liver RNA occurred without changing the liver DNA concentration. Kerosene exposure decreased the level of aspartate aminotransferase activities in serum ( P < 0.001) and liver ( P < 0.05) but it increased ( P < 0.05) the liver alanine aminotransferase activity without changing its activity in serum. The levels of serum ( P < 0.01) and liver ( P < 0.001) lactate dehydrogenase activity were declined and the serum ( P < 0.05) and liver ( P < 0.05) alkaline phosphatase activity levels were elevated in kerosene-treated fish. The nominated levels (3.33–6.66 ml/L) of kerosene significantly ( P < 0.01) elevated the thyroxine (T 4) titre, and reduced ( P < 0.05) the triiodothyronine (T 3) titre. The fish pretreated with either T 3 or T 4 and exposed to kerosene had a metabolic and thyroidal response that differed from that in control fish treated with kerosene: no rise in serum glucose was observed, nor in triglycerides, total protein and RNA in the liver, whereas declined levels of T 4 and T 3 were observed. The upregulation of the thyroid along with the marked metabolite changes point to a positive involvement of thyroid in energy metabolism during kerosene exposure. This is consistent with the hypothesis that the fish thyroid responds to the action of petroleum products and influences the metabolic homeostasis of this air-breathing fish.

Enzymatic responses to metal exposures in a freshwater fish Oreochromis niloticus

Freshwater fish Oreochromis niloticus were exposed to 5, 10 and 20 μM concentrations of Cd, Cu, Zn and Pb for 14 days and responses of several enzymes were determined subsequently. Liver catalase (CAT) activity was influenced by Cd and Pb exposures, while it was inhibited by Zn exposure. Copper, on the other hand, did not cause significant changes in CAT activity. Liver alkaline phosphatase (AP) activity was first stimulated at lowest (5 μM) exposure concentration, while there were significant inhibitions at higher (10 μM) exposure concentration. At the highest (20 μM) exposure concentration, AP activity was compensated coming to the control level, except Pb exposure. Intestine and serum AP activities were stimulated by all Zn exposures and 10 μM Cu exposure, while other exposures did not cause significant changes on AP activity. Na,K-ATPase activity in the gill and intestine was inhibited by all the metal exposures, except 20 μM Pb exposure that resulted in an increase in the activity in the gill. Similarly, muscle Ca-ATPase activity was inhibited by all the metal exposures, except Cu exposures. This study indicated that enzymatic systems may be used as a sensitive bioindicator of metal contamination in aquatic systems. Nevertheless, the results also stress the importance of addressing the sensitivity of these enzymes when they are used as a bioindicator for metal contamination, because the responses of the enzymes varied considerably according to metal types and concentrations.

Gender-based comparative toxicity of di-ethyl phthalate in Wistar rats

In recent years, the exposure of humans to phthalate esters through environmental contamination has increased. One among them is di-ethyl phthalate (DEP), which is used as a plastisizer for cellulose ester plastic films and sheets, solid rocket propellants, molded and extruded articles, as a component in insecticide sprays and various other substances, as well as in industrial applications. Release into the environment occurs primarily as a result of production and manufacturing of DEP and during the use and disposal of products containing DEP. Therefore, a study was undertaken to evaluate gender-specific toxicity of DEP in Wistar rats. Rats of both sexes, weighing 125–130 g, were administered 50 ppm (w/v) DEP in water ad libitum for a period of 180 days and were given normal diet. Control animals received normal diet and water ad libitum. During the treatment, rats were weighed every week and water consumption per day was measured. After the completion of treatment, liver weight : body weight−1 ratio, liver weight, body weight−1, liver and serum enzymes, and other biochemical parameters of liver and serum were assessed. It was observed that there was no significant change in body weight−1, liver weight, liver weight : body weight−1 ratio, and water consumption in both sexes. There were significant increases in liver acid phosphatase (ACP) activity and kidney glutathione levels, and nonsignificant changes in liver alkaline phosphatase (ALP), aspartate aminotransferase (AST), alanine aminotransferase (ALT), succinate dehydrogenase (SDH), and lactate dehydrogenase (LDH) activities in DEP-treated male rats, whereas in DEP-treated female rats the liver showed significant decrease in ALP and SDH and nonsignificant changes in AST, ALT, and LDH activities. Serum ACP and LDH levels in DEP-treated male rats were significantly decreased, and in the case of DEP-treated female rats, only serum LDH levels were significantly decreased. There was no significant change in serum ALP, AST, and SDH levels in DEP-treated male and female rats as compared to control rats. Histology of the livers of both male and female rats showed loss of hepatic architecture, degenerative changes in hepatocytes, and vacuolation in hepatocytes in both the centrilobular and periportal areas. It can be concluded from this study that prolonged exposure to DEP at 50 ppm levels can be harmful to animals and humans. This is evident from the present study as certain significant changes in enzyme activities in the liver, serum, and histological alterations in liver were observed.

Regulatory effect of divalent cations on rat liver alkaline phosphatase activity: &lt;I&gt;How Mg&lt;SUP&gt;2+&lt;/SUP&gt; activates (and inhibits) the hydrolysis of p-nitrophenylphosphate&lt;/I&gt;

The concentration-dependent stimulation of rat liver alkaline phosphatase (ALP) catalyzed hydrolysis of para- nitrophenylphosphate (pNPP) was studied. ALP displayed some activity even in the absence of exogenous Mg2+. Kinetic analyses show that activation by Mg2+ is exerted at the Vmax level without necessarily enhancing the affinity of the enzyme for the ion. However, the hyperbolic activation operates only within the optimal level of 0 to 5mM concentrations of the metal ion. Higher concentrations were actually inhibitory in a pure non-competitive manner. Mg2+, either as an activator (optimal concentrations) or inhibitor (supra-optimal levels) exerts its action via a Vmax effect with only negligible effect on Km for the substrate. Keywords: magnesium ion, alkaline phosphatase, supra optimal regulation Biokemistri Vol. 17(2) 2005: 129-136

Toxic effects of novel organophosphorus insecticide (RPR-V) on certain biochemical parameters of euryhaline fish, Oreochromis mossambicus

The euryhaline fish, Oreochromis mossambicus was exposed to sub-lethal concentration (0.017 mg L −1) of a novel phosphorothionate, 2-butenoic acid-3-(diethoxy phosphinothionyl) ethyl ester (RPR-V) for 30 days and allowed to recover for 7 days. Important biomarker enzymes were assayed in plasma, brain, gill, liver, kidney, and muscle during exposure tenures of day-3, -7, -15, -30, and also at 7 days (withdrawal) after stopping treatment. Acetylcholinesterase (AChE) activities of brain, gill, and muscle were strongly inhibited by 67, 75, and 66%, respectively, on day-30. Exposure (time) dependent increases in alanine aminotransferase (ALAT), and aspartate aminotransferase (ASAT), acid phosphatase (AcP), and alkaline phosphatase (AkP), activities in plasma and kidney; AcP and AkP activities in gill were noticed. However, significant decrease in ALAT, ASAT, AcP, and AkP activities in liver was observed. The depletion of glycogen was observed in liver, brain, and gill tissues, an indication of typical stress related response of the fish with pesticide. A significant increase in lactate dehydrogenase (LDH) activity in gill and brain was observed and decreased in liver and muscle, indicating tissue damage and muscular harm. Depletion of glutathione (GSH) was observed in the above tissues, there by enhancing the lipid peroxidation resulting in cell damage. The induction in hepatic glutathione- S-transferase (GST) levels indicates the protection against the toxicity of xenobiotic-induced lipid peroxidation. There was a significant recovery in all the above biochemical parameters, in all the tissues of fish after a recovery period of 7 days. These results revealed that RPR-V affects the intermediary metabolism of O. mossambicus and the increase of biomarker enzymes in plasma, might be due to the necrosis of liver.

Chronic Administration of Aqueous Extract of Hibiscus sabdariffa. Enhances Na+-K+-ATPase and Ca2+-Mg2+-ATPase Activities of Rat Heart

The effect of oral administration of an aqueous extract of Hibiscus sabdariffa. Linn petals on Na+-K+-ATPase and Ca2+-Mg2+-ATPase activities of rat heart have been investigated in Sprague-Dawley rats. The extract was administered orally in doses of 25.0 and 50.0 mg/kg body weight for 28 days. Results showed that Hibiscus sabdariffa. treatment led to significant increases (p < 0.001) of Na+-K+-ATPase and Ca2+-Mg2+-ATPase at both doses. Cardiac weight index of rats treated with H. sabdariffa. at a dose of 50 mg/kg body weight was significantly reduced (p < 0.01) compared with those of the control and rats treated with H. sabdariffa. at a lower dose. Administration of the extract at both doses did not show any signs of cardiotoxicity and hepatotoxicity as judged by biochemical “marker” enzymes (alkaline phosphatase, aspartate aminotransferase, and alanine aminotransferase) activities in plasma, heart, and liver of rats. These results demonstrate that aqueous extract of H. sabdariffa. enhances cardiac Na+-K+-ATPase and Ca2+-Mg2+-ATPase activities and supports the public belief that H. sabdariffa. may be a safe cardioprotective agent.

Increased liver alkaline phosphatase and aminotransferase activities following administration of ethanolic extract of &lt;i&gt;Khaya senegalensis&lt;/i&gt; stem bark to rats

The effect of daily, oral administration of ethanolic extract of Khaya senegalensis stem bark (2mg/kg body weight) for 18days on the alkaline phosphatase, aspartate and alanine aminotransferase activities of rat liver and serum were investigated. Compared with the control, the activities of liver alkaline phosphatase (ALP), alanine aminotransferase (ALT) and aspartate aminotransferase (AST) increased significantly for the 6 and 18 days period of extract administration (P 0.05). The results indicate that the ethanolic extract of Khaya senegalensis stem bark has brought about induction of synthesis of the liver enzymes studied which is an important biochemical symptom of cytolysis.

Early Alteration in Bone Metabolism in Epileptic Children Receiving Carbamazepine Monotherapy Owing to the Induction of Hepatic Drug—Metabolizing Enzymes

The purpose of this study was to investigate, by a prospective, self-controlled method, whether early treatment with carbamazepine monotherapy can alter bone metabolism in ambulatory epileptic children with adequate sun exposure, based on the determination of total serum alkaline phosphatase and its bone isoenzyme activities. Serum total alkaline phosphatase and its bone, liver, and intestinal isoenzyme activities were evaluated in 22 epileptic ambulatory children (13 males and 9 females, aged from 5 to 12 years) before and at 3, 6, and 12 months of carbamazepine monotherapy. Serum concentrations of other biochemical markers of bone and liver metabolism, such as calcium, phosphorus, magnesium, γ-glutamyltransferase, alanine aminotransferase, aspartate aminotransferase, and lactate dehydrogenase, were also measured in the study participants before and at 6 and 12 months of treatment. Carbamazepine was prescribed at normal dosages (16.4—20 mg/kg/day). Serum total alkaline phosphatase activities were significantly increased at 3 ( P = .000), 6 ( P = .024), and 12 ( P = .037) months of treatment; serum bone alkaline phosphatase activities at 3 ( P = .000), 6 ( P = .008), and 12 ( P = .017) months of treatment; and serum liver alkaline phosphatase activities at 3 ( P = .000), 6 ( P = .049), and 12 ( P = .008) months of treatment, whereas serum intestinal alkaline phosphatase isoenzyme activity was significantly increased only at 3 months of treatment ( P = .035). Serum γ-glutamyltransferase activities were also significantly increased at 6 ( P = .000) and 12 ( P = .000) months of treatment. No significant changes in the concentrations of serum calcium, phosphorus, magnesium, alanine aminotransferase, aspartate aminotransferase, and lactate dehydrogenase were noted at 6 and 12 months of treatment. There was a significant correlation between serum γ-glutamyltransferase activities and serum total alkaline phosphatase activities ( r = .689, P = .000 at 6 months; r = .493, P = .020 at 12 months), bone alkaline phosphatase activities ( r = .700, P = .000 at 6 months; r = .466, P = .029 at 12 months), and liver alkaline phosphatase activities ( r = .427, P = .047 at 6 months; r = .425, P = .048 at 12 months). These findings indicate that ambulatory children who receive carbamazepine monotherapy, even when residing in a country with adequate sunlight, can have their bone metabolism altered early in the course of treatment, as indicated by the elevated activities of serum bone alkaline phosphatase isoenzyme. This early alteration in bone metabolism is probably due to the hepatic enzyme—inducing character of carbamazepine. ( J Child Neurol 2005;20:513—516).

Early Alteration in Bone Metabolism in Epileptic Children Receiving Carbamazepine Monotherapy Owing to the Induction of Hepatic Drug-Metabolizing Enzymes

The purpose of this study was to investigate, by a prospective, self-controlled method, whether early treatment with carbamazepine monotherapy can alter bone metabolism in ambulatory epileptic children with adequate sun exposure, based on the determination of total serum alkaline phosphatase and its bone isoenzyme activities. Serum total alkaline phosphatase and its bone, liver, and intestinal isoenzyme activities were evaluated in 22 epileptic ambulatory children (13 males and 9 females, aged from 5 to 12 years) before and at 3, 6, and 12 months of carbamazepine monotherapy. Serum concentrations of other biochemical markers of bone and liver metabolism, such as calcium, phosphorus, magnesium, gamma-glutamyltransferase, alanine aminotransferase, aspartate aminotransferase, and lactate dehydrogenase, were also measured in the study participants before and at 6 and 12 months of treatment. Carbamazepine was prescribed at normal dosages (16.4-20 mg/kg/day). Serum total alkaline phosphatase activities were significantly increased at 3 (P = .000), 6 (P = .024), and 12 (P = .037) months of treatment; serum bone alkaline phosphatase activities at 3 (P = .000), 6 (P = .008), and 12 (P = .017) months of treatment; and serum liver alkaline phosphatase activities at 3 (P = .000), 6 (P = .049), and 12 (P = .008) months of treatment, whereas serum intestinal alkaline phosphatase isoenzyme activity was significantly increased only at 3 months of treatment (P = .035). Serum gamma-glutamyltransferase activities were also significantly increased at 6 (P = .000) and 12 (P = .000) months of treatment. No significant changes in the concentrations of serum calcium, phosphorus, magnesium, alanine aminotransferase, aspartate aminotransferase, and lactate dehydrogenase were noted at 6 and 12 months of treatment. There was a significant correlation between serum gamma-glutamyltransferase activities and serum total alkaline phosphatase activities (r = .689, P = .000 at 6 months; r = .493, P = .020 at 12 months), bone alkaline phosphatase activities (r = .700, P = .000 at 6 months; r = .466, P = .029 at 12 months), and liver alkaline phosphatase activities (r = .427, P = .047 at 6 months; r = .425, P = .048 at 12 months). These findings indicate that ambulatory children who receive carbamazepine monotherapy, even when residing in a country with adequate sunlight, can have their bone metabolism altered early in the course of treatment, as indicated by the elevated activities of serum bone alkaline phosphatase isoenzyme. This early alteration in bone metabolism is probably due to the hepatic enzyme-inducing character of carbamazepine.

Effect of dietary microbial phytase supplementation on growth and nutrient digestibility of Pangasius pangasius (Hamilton) fingerlings

A feeding trial was conducted for 60 days to study the effects of exogenous microbial phytase supplementation on the growth and nutrient digestibility of Pangasius pangasius fingerlings. Eight isocaloric and isoprotein experimental diets (35.67% crude protein and 3870 kcal kg−1) were prepared with graded levels of phytase, e.g., 0 (T1), 150 (T2), 250 (T3), 350 (T4), 500 (T5), 1000 (T6) and 2000 (T7) FTU (phytase units) kg−1. Three hundred and fifteen fingerlings of P. pangasius (1.97–2.05 g) were randomly distributed in seven treatments with three replicates each. Maximum weight gain (350.72%), specific growth rate (2.51%), protein efficiency ratio (2.1), apparent net protein utilization (27.85%), energy retention value (88.47%) and feed conversion efficiency were observed in T5 group supplemented with 500 FTU phytase kg−1 diet. Apparent dry matter and protein digestibility in phytase-supplemented groups were significantly (P<0.01) higher at a minimum supplement of 500 FTU kg−1 or higher. Liver alkaline phosphatase activity increased significantly in treatment groups. Supplementation at 500 FTU kg−1 of phytase is optimum in the diet of P. pangasius fingerlings.

Suppression of diethylnitrosamine and 2-acetylaminofluorene-induced hepatocarcinogenesis in rats by tocotrienol-rich fraction isolated from rice bran oil

The anticancer efficacy of tocotrienol-rich fraction (TRF) was evaluated during diethylnitrosamine (DEN)/2-acetylaminofluorene (AAF)-induced hepatocarcinogenesis in male Sprague-Dawley rats. TRF treatment was carried out for 6 months, and was started 2 weeks before initiation phase of hepatocarcinogenesis. Morphological examination of the livers from DEN/AAF rats showed numerous off-white patches and few small nodules, which were significantly reduced by TRF treatment. Cytotoxic damage by DEN/AAF was estimated by alkaline phosphatase (ALP) release into the plasma from the cell membranes. DEN/AAF caused a twofold increase in the activity of ALP in plasma as compared with normal control rats, and this increase was prevented significantly by TRF treatment. We observed an increase of 79% in liver ALP activity in DEN/AAF rats, which was further increased by another 48% after the administration of TRF. Hepatic activity of glutathione S-transferase (GST) was also increased (3.5-fold) during the induction of hepatic carcinogenesis. Lipid peroxidation and low-density lipoprotein (LDL) oxidation increased threefold following initiation by DEN/AAF as compared with normal control rats. However, TRF treatment to DEN/AAF-treated rats substantially decreased (62-66%) the above parameters and thus limited the action of DEN/AAF. We conclude that long-term intake of TRF could reduce cancer risk by preventing hepatic lipid peroxidation and protein oxidation damage due to its antioxidant actions.

Growth and dietary utilisation in goldfish ( Carassius auratus Linn.) fed diets formulated with various local agro-produces

During a 60 d feeding trial, goldfish ( Carassius auratus) measuring 1.66 ± 0.02 g by weight and 4.2 ± 0.02 mm by length were fed diets containing 23.34%, 26.21%, 29.30%, 32.24% and 42.53% crude protein in Feeds I through V respectively. The four formulated-diets (Feeds I, II, IV and V) contained groundnut oil-cake, wheat bran, soybean meal, fish meal, cod liver oil, vegetable oil and vitamin–mineral mixture with tapioca as binder and a commercially-available diet (Feed III) procured from the market. All the feeds were dispensed twice daily at 4% body weight. Results revealed that the growth (in terms of net weight gain and specific growth rate) and dietary utilisation (in terms of feed conversion ratio, protein retention efficiency and energy retention efficiency) were observed to be significantly greater ( p ⩽ 0.05) in Feed V which contained 42.53% protein followed by Feeds IV, I, II and III, and 7.58%, 6.11%, 6.63%, 7.86% and 7.91% lipid in Feeds I through V, describing clearly the role of a combination of protein and lipid in the diet for growth and feed utilisation. Lowest growth and dietary utilisation was observed in Feed III (the commercial diet). The alkaline and acid phosphatase activities in liver, gill and intestine as also the RNA:DNA ratio in the muscle tissues were greatest in fish fed Feed V, which indicated best growth. It was thus concluded that a protein content of 40–45% in the diet of young goldfish could significantly enhance growth and dietary utilisation.

成長期ラット唾液腺における亜鉛酵素の性質に関する研究

Zinc (Zn) has been known to be an essential metal and is very important for growth and cell division. Zn is required for activities of more than 300 enzymes. In our previous studies, we used rats to study the effect of low intakes of zinc and calcium on the growth and development in tibia metaphysis. However we have no report on the enzyme for cofactor zinc in rats. Twenty, three-week-old male Wistar rats were divided into groups and randomly given a diet containing different levels of zinc (adequate Zn level 34.4ppm), high-Zn diet (Zn level 51.4ppm), low-Zn diet (14.7ppm), and Zn-deficiency (Zn level 3.7ppm) for 6 weeks. We examined the properties of the enzyme for cofactor zinc enzyme (alkaline phosphatase and Cu, Zn superoxide dismutase) in serum, liver and salivaly glands. 1. Serum concentrations of Zn did not show a significant difference among the four groups. 2. In the high-Zn and low Zn diet groups, alkaline phosphatase activity in serum and liver was increased in conparison to the control group, however, in submandibular glands and sublingual glands it was decreased as compared with the control group. 3. The Cu, Zn-superoxide dismutase activity in liver did not show a significant difference among the four groups. In the low-Zn and Zn deficiency diet groups, the type of Cu, Zn-Super oxide dismutase activity in submandibular glands was decreased as compared with the control group ; on the other hand, in the high-Zn, low-Zn and Zn deficiency diet groups, Cu, Zn-superoxide dismutase activity in sublingual glands and parotid glands was decreased as compared with the control group. These results suggested that the enzyme activities of alkaline phosphatase and type of Cu, Zn-superoxide dismutase were not dependent on the level of zinc present in the diet of each of the four groups, particularly under normal physiological zinc levels.

Kinetics of mRNA expression of alkaline phosphatase isoenzymes in hepatic tissues from glucocorticoid-treated dogs.

To clone segments of the canine liver alkaline phosphatase (LALP) and corticosteroid-induced alkaline phosphatase (CIALP) genes and use those clones to determine the tissue source of CIALP, the kinetics of LALP and CIALP mRNA expression for glucocorticoid-treated dogs, and the correlation between LALP and CIALP transcript concentrations and isoenzyme activities. Tissues obtained from 7 dogs treated with prednisone (1 mg/kg, SC, q 24 h) for up to 32 days and 1 untreated (control) dog. Gene segments of LALP and CIALP were obtained by reverse transcription-polymerase chain reaction (RT-PCR) assay. The tissue source of CIALP and IALP mRNA was determined by northern blot analysis of tissues from 1 of the glucocorticoid-treated dogs. Hepatic tissues and serum samples were obtained from the 6 remaining glucocorticoid-treated dogs on days 0, 2, 5, 10, and 32 of prednisone treatment, and relative expression of LALP and CIALP mRNA was correlated with LALP and CIALP activity. A 2,246-base pair (bp) segment of canine LALP and a 1,338-bp segment of CIALP were cloned. Northern blot analysis revealed CIALP mRNA expression in hepatic tissues only after glucocorticoid treatment. Kinetics of LALP and CIALP mRNA expression in the liver of glucocorticoid-treated dogs paralleled liver and serum activities of LALP and CIALP. The liver is the most likely source for CIALP in dogs. Analysis of kinetics of serum and hepatic LALP and CIALP mRNA suggests that after glucocorticoid treatment, both are regulated by modification of mRNA transcript concentrations, possibly through differing mechanisms.

Canine Motor Neuron Disease: Clinicopathologic Features and Selected Indicators of Oxidative Stress

Hereditary canine spinal muscular atrophy (HCSMA) is an inherited motor neuron disease affecting a kindred of Brittanies. We have examined the clinicopathologic abnormalities in 57 animals with HCSMA, including 43 affected adult dogs and 14 homo‐zygote pups. We also measured selected biochemical indices of oxidative stress: serum vitamin E (α‐tocopherol) and Se concentrations; serum concentrations of Cu, Zn, Mg, and Fe; and total superoxide dismutase and glutathione peroxidase activities in red blood cells. Dogs with HCSMA had the following abnormalities: regenerative anemia, hypoglobulinemia, hypochloremia, and abnormally high creatine kinase and liver alkaline phosphatase activities. Serum Cu concentration was significantly (P= .01) increased in adult dogs with HCSMA compared to control dogs. Serum vitamin E concentrations tended to be lower in adult dogs with HCSMA compared to controls, and were significantly (P= .01) lower in homozygote pups compared to control pups.

Canine motor neuron disease: clinicopathologic features and selected indicators of oxidative stress.

Hereditary canine spinal muscular atrophy (HCSMA) is an inherited motor neuron disease affecting a kindred of Brittanies. We have examined the clinicopathologic abnormalities in 57 animals with HCSMA, including 43 affected adult dogs and 14 homozygote pups. We also measured selected biochemical indices of oxidative stress: serum vitamin E (alpha-tocopherol) and Se concentrations; serum concentrations of Cu, Zn, Mg, and Fe; and total superoxide dismutase and glutathione peroxidase activities in red blood cells. Dogs with HCSMA had the following abnormalities: regenerative anemia, hypoglobulinemia, hypochloremia, and abnormally high creatine kinase and liver alkaline phosphatase activities. Serum Cu concentration was significantly (P = .01) increased in adult dogs with HCSMA compared to control dogs. Serum vitamin E concentrations tended to be lower in adult dogs with HCSMA compared to controls, and were significantly (P = .01) lower in homozygote pups compared to control pups.

Semiautomated analysis of alkaline phosphatase isoenzymes in serum of normal cynomolgus monkeys (Macaca fascicularis).

Alkaline phosphatase (ALP) isoenzyme analysis, using a combination of wheat germ lectin (WGL) precipitation, levamisole inhibition and an automated p-nitrophenylphosphate assay was validated for use with serum from monkeys (Macaca fascicularis) and used to determine the activities of liver ALP (LALP), bone ALP (BALP) and intestinal ALP (IALP). Based on serial dilution studies and within-run and between-run coefficients of variation, each assay had excellent linearity and acceptable precision. In addition, liver and intestinal mucosa extracts for tissue specific alkaline phosphatases were used to confirm assay validations. Gender-specific differences for total ALP, LALP, and BALP activities were present in sera from normal monkeys between 2 and 4 years of age. Males had 1.3-fold higher total ALP and LALP activities, and 1.5-fold higher BALP activity compared with females. The majority of ALP activity in normal monkey serum was LALP isoenzyme activity, which ranged from 56.7% to 94.7% of total activity. Serum BALP activity ranged from 5.3% to 42.8%. There was negligible IALP activity in all serum samples.

Effect of ascorbic acid supplementation on liver and kidney toxicity in cyclophosphamide-treated female albino rats.

Effects of ascorbic acid supplementation on the activity of acid phosphatase (ACP), alkaline phosphatase (ALP), glutamic oxaloacetic transaminase (GOT) and glutamic pyruvic transaminase (GPT) on liver, kidney and serum in cyclophosphamide-treated female virgin rats were investigated. Oral administration of cyclophosphamide at the dose of 5 mg/kg body weight/day for 12 days resulted in a significant elevation in ACP and ALP activities in liver, kidney and serum. Ascorbic acid supplementation at the dose of 25 mg/kg body weight/day showed a significant protection in the activity of ACP in liver, kidney and serum, but only in ALP activity in kidney. ALP activities in liver and serum were not restored to control level by ascorbic acid supplementation. Activities of GOT and GPT were elevated significantly in liver, kidney and serum after cyclophosphamide treatment, and were protected and restored to control level by ascorbic acid supplementation.

Further investigations into the bioactivity of root extract of Plumbago zeylanica

The metabolic effect of crude and ethanol extracts of the root of Plumbago zeylanica was investigated in rats. The treatment of rats with crude Plumbago zeylanica and its ethanol extract resulted in an increase in the activities of serum lactate dehydrogenase, acid phosphatase and liver alkaline phosphatase. The blood sugar concentrations increased significantly while liver acid phosphatase and total nucleic acids were drastically reduced.

Heavy metal chromium induced alterations on phosphatases activity in the Indian major carp, Catla catla (HAM.)

Tissue homogenates of the Indian riverine major carp Catla catla revealed the extent of alkaline phosphatase activity to be higher than that of acid phosphatase activity. Phosphatases activity as a function of sublethal concentrations of chromium evidenced a general decline reflecting injury to lysosome due to stress in the biological system. Dose as well as exposure period dependent statistically significant (p<0.05) inhibition in acid phosphatase activity in liver and intestine, and alkaline phosphatase activity in muscle, liver, gill and intestine of Catla catla are advocated as bioindicators of water borne heavy metal chromium stress.