Alkaline Phosphatase Activity In Rats Research Articles

Quercetin and hesperidin protection against hepato-renal damage occasioned by carbon tetrachloride (CCL4) in a rat model

BackgroundCurrent pharmacological research has shown that medicinal plants have notable bioactivities. For more than a millennium, traditional Chinese medicine (TCM) has prescribed CRP primarily as a qi-regulating medication for therapeutic purposes. Hence, the synergistic effect of the two medicinal plants on the hepato-renal damage in rats exposed to CCL4. Materials and MethodsFor twenty-one days, rats were gavaged with quercetin and hesperidin (2.4 and 2.4 mg/kg each) after being exposed to CCL4 (0.5 mg/kg). Samples were taken to evaluate several biochemical markers. Nitric oxide (NO), hydrogen peroxide (H2O2), and malondialdehyde (MDA) were measured. The activity of the enzymes alanine transferase (ALT) and alkaline phosphatase (ALP) were estimated to represent liver function. Catalase (CAT), Glutathione peroxidase (GPx), and Glutathione (GSH) levels were evaluated for antioxidant level, total bilirubin, total protein, urea, uric acid, and creatinine), as well as histopathology were assessed. ResultsThe concentration of total bilirubin, total protein, urea, uric acid, creatinine, increased considerably (P < 0.05) after exposure to carbon tetrachloride, with the levels of H2O2, MDA, SOD, CAT, GPX, GSH, and the activities of ALT and AST in serum, also, changes observed in histopathological findings. Upon treatment with the extracts, the levels of H2O2 and MDA was significantly (P < 0.05) reduced and modify SOD, CAT, GPX, GSH, ALT, and ALP activities in rats substantially (P < 0.05). With slid changes on histopathological effect. ConclusionQuercetin and hesperidin treatment successfully improved liver and kidney pathophysiology and reduce the level of ROS. Thus, quercetin and hesperidin can be recommended as a hepato-renal preventive agent against CCL4-induced toxicity.

High-fat diet promotes the effect of fructo-oligosaccharides on the colonic luminal environment, including alkaline phosphatase activity in rats

We recently reported that fermentable nondigestible carbohydrates such as oligosaccharides, commonly increase colonic alkaline phosphatase (ALP) activity and the gene expression of Alpi-1, coding for rat intestinal alkaline phosphatase-I isozyme in rats and that the effect of oligosaccharides on colonic ALP activity is affected by the quality of dietary fats. We hypothesized that the amount of dietary fat would modulate the effect of oligosaccharides on colonic ALP and luminal environment in rats. In experiment 1, male Sprague-Dawley rats were fed a low-fat (LF, 5% lard) or high-fat (HF, 30% lard) diet with or without 4% fructo-oligosaccharides (FOS). In experiment 2, they were fed a 2.5%, 7%, 20%, or 40% fat (lard) diet with 4% FOS for 2 weeks. Dietary FOS in the HF diet (HF-FOS) significantly increased ALP activity in the colon and cecal digesta and colonic expression of Alpi-1, but not in the LF diet with FOS groups (LF-FOS). In comparison to the LF-FOS group, the increases in fecal mucins, Lactobacillus ratio, as well as cecal n-butyrate, and the decrease in fecal Clostridium coccoides, were more pronounced in the HF-FOS group. Compared with the 2.5% or 7% fat + FOS diet, the 20% fat + FOS diet significantly increased colonic ALP activity, Alpi-1 expression, and fecal mucins. These factors did not differ significantly between 20% and 40% fat + FOS diets. To exert the maximum effect of FOS on the colonic luminal environment, including ALP activity in rats, significantly more fat may be required than that contained present a LF diet.

AntagomiR-29b inhibits vascular and valvular calcification and improves heart function in rats.

We aimed to investigate the role of the miR‐29b and its effect on TGF‐β3 pathway in vascular and valvular calcification in a rat model of calcific aortic valve diseases (CAVD). A rat model of CAVD was established by administration of warfarin plus vitamin K. The expression levels of miR‐29b, osteogenic markers and other genes were determined by qRT‐PCR, Western blot and/or immunofluorescence and immunohistochemistry. The calcium content and alkaline phosphatase (ALP) activity were measured. The calcium content, ALP activity and osteogenic markers levels in calcified aorta and aortic valve were augmented compared to controls. The expression of miR‐29b, p‐Smad3, and Wnt3 and β‐catenin was significantly up‐regulated, whereas TGF‐β3 was markedly down‐regulated. However, compared with the CAVD model group, the calcium content and ALP activity in rats treated with antagomiR‐29b were significantly decreased, and antagomiR‐29b administration reversed the effects of CAVD model on the expression of miR‐29b and osteogenic markers. Inhibition of miR‐29b in CAVD rats prevented from vascular and valvular calcification and induced TGF‐β3 expression, suggesting that the miR‐29b/TGF‐β3 axis may play a regulatory role in the pathogenesis of vascular and valvular calcification and could play a significant role in the treatment of CAVD and other cardiovascular diseases.

The effects of different high-fat (lard, soybean oil, corn oil or olive oil) diets supplemented with fructo-oligosaccharides on colonic alkaline phosphatase activity in rats.

We recently reported that fermentable non-digestible carbohydrates including fructo-oligosaccharides (FOS) commonly elevate colonic alkaline phosphatase (ALP) activity and the expression of IAP-I, an ALP gene, in rats fed a high-fat (HF) diet, and also elevate gut mucins and modulate gut microbiota. This study aims to investigate whether dietary fat types influence the effect of FOS on colonic ALP activity and the luminal environment in HF-fed rats. Male Sprague-Dawley rats were fed a diet containing 30% soybean oil, corn oil, olive oil or lard with or without 4% FOS for 2weeks. Colon ALP activity, gene expression, and gut luminal variables including mucins and microbiota were measured. In the lard diet groups, dietary FOS significantly elevated colonic ALP activity and the expression of IAP-I. The elevating effect of FOS on colonic ALP activity was also observed in the olive oil diet groups, although here the IAP-I expression was not changed. However, the soybean oil and corn oil diet groups did not exhibit the elevating effect of FOS on colon ALP. Fecal ALP and mucins were significantly elevated by dietary FOS regardless of dietary fat types, and the effect of FOS was prominent in the lard diet groups. The number of Lactobacillus spp. observed in fecal matter was significantly increased by dietary FOS in the lard and olive oil diet groups, but not in the soybean oil and corn oil diets groups. This study suggests that dietary fat types may change the effect of FOS on the colonic luminal environment including the ALP activity in rats fed a high-fat diet.

Expression characteristics of adiponectin and receptor activator of nuclear factor kappa B ligand in the alveolar bone of rats with periodontitis and its effect

ABSTRACT We sought to investigate the expression characteristics of adiponectin (APN) and receptor activator of nuclear factor kappa B ligand (RANKL) in the periodontal tissues of rats with periodontitis and the effect on vascular calcification. Thirty-six Sprague Dawley rats were randomly divided into a normal control group, periodontitis group, and vascular calcification group. Western blotting was employed to detect the expressions of APN and RANKL in the periodontal tissues of rats. Calcium content and alkaline phosphatase activity in the vascular tissue of rats were determined. Compared to the normal control group, the periodontitis and vascular calcification groups presented lower expressions of APN and RANKL. The expression of APN in the periodontal tissues of rats in the vascular calcification group was significantly lower than that in the periodontitis group. As for the calcium content and alkaline phosphatase activity in rats’ vascular tissues, the vascular calcification group displayed significantly higher rates than the other two groups, whereas the periodontitis group presented lower calcium content and alkaline phosphatase activity than the normal control group. APN and RANKL may be involved in the process of periodontitis and vascular calcification in rats, and some kinds of relationship may exist between periodontitis and vascular calcification.

Protective effect of zinc on the Alkaline Phosphatase Activity in rats exposed to Arsenic

Background: Considering the importance of the alkaline phosphatase enzyme for growth of liver cells and the presence of zinc in this regard the purpose of this project was to evaluate the Protective effect of zinc on the Alkaline Phosphatase Activity in rats exposed to Arsenic. Methods: In this experimental study, a total of 48 male Wistar rats were randomly allocated into 8 sub-groups and were categorized as two short and long term evaluation: in a short-term period: group 1 control, group 2 received 40 mg/l As sodium, group 3 received 40 mg/l As sodium and zinc simultaneously and group 4 received 40 mg/l Zn. in a long-term period groups group 1 control, group 2 received 20 mg/l As sodium, group 3 received 20 mg/l As sodium and zinc simultaneously and group 4 received 20 mg/l Zn with oral administration. Blood samples were taken over a 30-day and 60-day period and serum enzyme alkaline phosphatase was measured. Results: Administration of 2 different doses of as sodium decreased the activity of alkaline phosphatase compared to the control group. Moreover, the simultaneous use as sodium with zinc increased the activity of alkaline phosphatase (P<0/05). Conclusion: The arsenate sodium reduced the activity of alkaline phosphatase, and zinc can be able to reduce the toxic effects of arsenate sodium.

Evaluation of the serum sex hormones levels and alkaline phosphatase activity in rats’ testis after administering of berberine in experimental varicocele

Current study was aimed to investigate the protective effect of berberine (BB) on the serum gonadotropin-releasing hormone (GnRH), follicle-stimulating hormone (FSH), luteinizing hormone (LH), inhibin B (INHB), testosterone (T) and alkaline phosphatase (Alk-p) activity in the testis of experimental varicocele-induced animals. For the current objective, 30 mature-male Wistar rats were randomly divided into control (n = 6 rats), control-sham (n = 6 rats) and experimental groups (n = 18 rats). The animals in the experimental groups were undergone experimental varicocele and simple laparotomy was conducted in control-sham group. 60 days after varicocele (VCL) induction the experimental group subdivided into: non-treated VCL-induced and 50 mg/kg and 100 mg/kg BB-treated groups (intra-peritoneally). Following 60 days, the animals were euthanized and serum levels of testosterone and testicular activity of alkaline phosphatase were measured. Non-treated VCL-induced animals indicated a significant (P < 0.05) reduction in serum levels of T and INHB and a remarkable (P < 0.05) increase in GnRH, FSH, LH and Alk-p activity compared to control and control-sham groups. Insignificant changes were found between control and control-sham groups. Meanwhile, each BB administered group showed a remarkable (P < 0.05) increase in serum levels of T and INHB and a significant (P < 0.05) decrease in GnRH, FSH, LH and alkaline phosphatase activity in testis tissue. According to the current findings, BB by increasing serum levels of testosterone and INHB increases the testicular endocrine capacity and protects Leydig cell against inflammatory and oxidant injury of varicocele. In addition, BB by inhibiting GnRH, FSH, LH and alkaline phosphatase activity, regulate the levels of serum sex hormones in experimental varicocele and reduces varicocele-induced inflammatory reactions.

Effect of neonatal β(3)-adrenoceptor agonist CL 316,243 treatment on body fat accumulation and intestinal alkaline phosphatase activity in rats from reduced nests.

The aim of this study was to evaluate the effects of early life administration of β3-adrenoceptor agonist (CL 316,243) on somatic and feeding parameters, obesity development as well as small intestinal enzyme activity in 21- and 40-day-old overfed male Sprague-Dawley rats. To induce postnatal overnutrition, litter size was reduced to 4 pups/litter (small litters, SL); while in normally-nourished groups (NL) the litter size was adjusted to 10 pups/litter. From days 5 to 15, half of the suckling pups from NL and SL groups received CL 316,243 subcutaneously. From 21st to 40th day, in the post-weaning period, both control (NL, SL) and CL 316,243-treated (NL-CL, SL-CL) rats had free access to standard diet and water. Body composition was determined by magnetic resonance imaging, blood pressure was measured using non-invasive tail-cuff, and intestinal alkaline phosphatase (AP) activity was assessed by histochemistry. At 21 and 40 days of age the SL rats showed higher body mass, displayed higher adiposity and had significantly increased duodenal and jejunal AP activity compared with NL animals. On day 21, NL and SL rats treated with CL 316,243 showed significantly less fat deposition and jejunal AP activity than the non-treated controls. In contrast, treatment-related changes in adiposity and AP activity were not observed in 40-day-old NL-CL, SL-CL rats. These results indicate that early pharmacological intervention with CL did not permanently influence physiological processes involved in body weight/fat regulation, which resulted in the development of early-programmed overweight status in SL rats after weaning.

Effect of Selenium Supplementation on Serum Amylase, Lactate Dehydrogenase and Alkaline Phosphatase Activities in Rats Exposed to Cadmium or Lead

Abstract The purpose of the study was to assess the effect of selenium supplementation on serum amylase, lactate dehydrogenase (LDH) and alkaline phosphatase (ALP) activities in rats, during subacute exposure to toxic doses of cadmium or lead through the drinking water. The experimental groups (n=6) were: Control, Se (Se+4: 0,2 mg/l), Cd (Cd+2: 150 mg/l), Pb (Pb+2: 300 mg/l), Cd+Se (Cd+2: 150 mg/l; Se+4: 0,2 mg/l) and Pb+Se (Pb+2: 300 mg/l; Se+4: 0,2 mg/l). The animals were sacrificed after 56 days. Amylase, LDH and ALP activities were determined from serum. Se and Pb treatments caused an increase in amylase and LDH activities, when compared to Control group while Cd caused an increase in amylase activity and a decrease in LDH and ALP activities. Cd+Se caused a decrease in amylase activity and an increase in LDH activity, when compared to Cd. Pb+Se caused a decrease in amylase activity in comparison to lead. Selenium supplementation alleviated cadmium or lead induced changes in serum amylase activity. Selenium, coadministered with cadmium, caused a marked increase in serum LDH activity, when compared to cadmium alone or Control group while practically it had no effect on lead induced changes in LDH activity. Cadmium and lead induced disturbances in serum ALP activity were not influenced by selenium supplementation.

高脂肪食摂取ラットのアルカリホスファターゼ活性に及ぼすビタミンK&lt;sub&gt;2&lt;/sub&gt;（メナキノン）摂取の影響

高脂肪食摂取ラットのアルカリホスファターゼ活性に及ぼすビタミンK&lt;sub&gt;2&lt;/sub&gt;（メナキノン）摂取の影響

Influence of High-Phosphorus or High-Salt Feeding on Intestinal Alkaline Phosphatase Activity in Rats

Influence of High-Phosphorus or High-Salt Feeding on Intestinal Alkaline Phosphatase Activity in Rats

Effect of zinc deficiency and experimental diabetes on glutamate oxaloacetate, glutamate pyruvate aminotransferases and alkaline phosphatase activities in rats

The aim of this study was to investigate the effect of low dietary zinc intake and experimental diabetes on transaminases andalkaline phosphatase activities in rats. 8 week old male normal albino (Wistar) rats were fed diets containing either adequate(54 mg/kg) or deficient (1 mg/kg) quantities of zinc for one week. Ten rats from each group (n = 20) were injected withalloxan to induce diabetes. Control and alloxan rats were fed for three weeks and food intake and body weight gain wererecorded daily and twice weekly, respectively. On day 28 the animals were killed and blood glucose, serum zinc, pancreaticzinc, serum glutamate oxalate transaminase (GOT), serum glutamate pyruvate transaminase (GPT) and serum alkalinephosphatase were determined after an overnight fast. Body weight gain of diabetic animals at the end of four weeks of dietarymanipulation was significantly lower than those of the non-diabetic animals. Diabetic rats had higher food intake and lowerserum and pancreatic zinc concentrations compared with non-diabetic rats. Dietary zinc intake significantly altered the bodyweight gain, food intake and serum zinc concentration of diabetic or non-diabetic rats. Serum GOT and GPT weresignificantly higher in alloxan-induced diabetic rats than in normal rats while the level of serum alkaline phosphatase waslower. The consumption of low-Zn diet led to increase in GOT and GPT, and decrease in serum alkaline phosphatase. Inconclusion, the combination of zinc deficiency and diabetes affects the activities of GOT, GPT and alkaline phosphatase, andit appears that zinc deficiency may lead to the development of severe diabetes.

Changes of heme oxygenase-carbon monoxide system in vascular calcification in rats

The aim of the present study was to investigate the change in heme oxygenase (HO)-carbon monoxide (CO)-cyclic guanosine monophosphate (cGMP) pathway in vascular calcification. Vascular calcification model was established in rats by using vitamin D 3 and nicotine. Vascular calcium content, alkaline phosphatase (ALP) activity, HO activity, HbCO formation and content of cGMP in vessels were measured. Immunochemistry (IH) for HO 1 expression and in situ hybridization (ISH) for HO 1 mRNA were observed. Compared to those of control rats, the aortic calcium content and vascular ALP activity in rats of the calcified group (VDN group) were obviously increased, but HO 1 activity, CO concentration and cGMP content in vessels of rats in VDN group were markedly decreased. Expressions of HO-1 protein and mRNA were significantly decreased compared to control rats. Vascular calcification might induce a down regulation in vascular HO-CO-cGMP pathway.

Effects of adrenomedullin on vascular calcification in rats.

The aim of the present study was to investigate the effect of adrenomedullin (ADM) on vascular calcification. The vascular calcification model was established in rats (VND group) by using vitamin D3 (300,000 IU/kg) and nicotine (25 mg/kg, two doses). The effect of liposome-encapsulated ADM was observed. Vascular calcium content, alkaline phosphatase (ALP) activity, ADM in aortic tissue and plasma, binding ability of 125I-ADM for ADM receptor on vascular plasma membrane and content of cAMP in vessels were measured. Compared with control rats, the aortic calcium content and vascular ALP activity in rats of the VDN group was obviously increased; in addition ADM concentrations in plasma and vessels of rats in VDN group were increased. But the maximum binding sites of 125I-ADM for ADM receptor (Bmax) on vascular plasma membrane in rats of VDN group were significantly decreased compared with control rats. The affinity of 125I-ADM for the ADM receptor was reduced, as shown by the Kd value and vascular cAMP content being reduced in rats of the VDN group compared to the control group. The in vitro response of isolated vessels to ADM incubation was weakened. Administration of empty liposome had no effect on vascular calcification. But administration of ADM significantly decreased vascular calcium content and ALP activity. The Bmax of 125I-ADM for ADM receptors on vascular plasma membrane increased by 17.7% (p < 0.01), and the value of Kd decreased by 36.2% (P < 0.01) in rats treated with ADM as compared with rats of the VDN group. In addition, the vascular cAMP content and the response to ADM in isolated aorta were markedly increased. Vascular calcification induced an alteration of the vascular ADM-ADM receptor-cAMP pathway. Treatment with exogenous ADM inhibited vascular calcification by improving the vascular ADM-ADM receptor-cAMP pathway.

A Possible Mechanism of Increase in Serum Alkaline Phosphatase Activity in Rats Given Granulocyte Colony-Stimulating Factor.

Recombinant human granulocyte colony-stimulating factor (G-CSF) at a dose of 1 to 300 micrograms/kg/day was administered intravenously to rats daily for 13 weeks. Serum alkaline phosphatase (ALP) activity increased dose-dependently with leukocytosis. Most of the increased leukocytes were segmented neutrophils, and neutrophil alkaline phosphatase (NAP) scores were elevated markedly. Serum ALP activity correlated very well with the segmented neutrophil counts, and the coefficient of correlation was more than 0.97 in both sexes. Pathological examinations revealed splenomegaly and a marked increase in neutrophils in the red pulp of the spleen. In the spleen, phagocytosis of neutrophils by macrophages was observed. These data indicate that the increased ALP was of neutrophil origin. Serum ALP activity may be increased by the direct release of ALP from the high number of neutrophils into the blood, or by the leakage of ALP into the blood mainly from the spleen where many neutrophils are pooled and destroyed by the macrophage system.

Preventive effect of beta-alanyl-L-histidinato zinc on bone metabolism in rats fed on low-calcium and vitamin D-deficient diets.

The effect of beta-alanyl-L-histidinato zinc (AHZ) on bone metabolism in the femoral diaphysis of rats fed on low-calcium and vitamin D-deficient diets was investigated. Rats were orally administered AHZ (10, 30, and 100 mg/kg per day) for 14 days and were killed on the 15th day. Feeding with low-calcium and vitamin D-deficient diets caused a significant decrease in serum 25-hydroxy-vitamin D3, calcium, and inorganic phosphorus concentrations. These decreases were not prevented by AHZ administration. Meanwhile, the femoral-diaphyseal calcium and phosphorus contents were significantly reduced by feeding with the deficient diets. Decrease in bone calcium content was significantly prevented by the doses of 30 and 100 mg AHZ/kg. Furthermore, the dose of 100 mg AHZ/kg produced a significant increase in bone deoxyribonucleic acid (DNA) content and alkaline phosphatase activity in rats fed on the deficient diets. Bone zinc content in the deficient rats was significantly increased by the doses of AHZ (30 and 100 mg/kg). The present results suggest that oral administration of AHZ has a preventive effect in the development of deteriorating bone metabolism in rats fed on low-calcium and vitamin D-deficient diets.

Effect of Duodenal Ulcerogens Mepirizole and Propionitrile on Small Intestinal and Liver Alkaline Phosphatase Activity in Rats

Duodenal ulcer could be induced in rats by a single subcutaneous injection of the anti-inflammatory agent mepirizole (M) or by the alkyl chemical propionitrile (P). Contrary to M, P provokes HCl hypersecretion as well. We used these animal models of duodenal ulcer to study the preulcerogenic molecular changes in the mucosal cells and their causal relationship to HCl hypersecretion. It was found that M and P induced the dose- and time-dependent decrease of duodenal alkaline phosphatase (DAP) activity. The decrease was detected at 4 h, with a nadir at 12 h after the injection of both drugs. The decrease of alkaline phosphatase activity was organ-specific after P administration and it was even regional-specific along the small intestine after M administration. At the level of mucosal cells of duodenum the effect of the ulcerogens was enzyme-selective. Both ulcerogens decreased protein and alkaline phosphatase activities; however, they had no effect on lysosomal acid phosphatase. Contrary to cysteamine (C), the effect of M and P on DAP depletion could not be reproduced under in vitro conditions. An interference of P and a slight additive effect of C on DAP depletion after simultaneous subcutaneous administration with M to the rats was found. The results indicate that the DAP depletion after in vivo administration of the three duodenal ulcerogens could be provoked by at least two different mechanisms. The decrease of DAP activity seems to be a general property of the duodenal ulcerogens independent of their effects on gastric acid secretion or on the suppression of alkaline secretion in the duodenum. As a late molecular event most probably elicited by the early morphological changes, the decrease of DAP activity could rather be related to ulcer healing than to its pathogenesis.

Benzene-specific increase in leukocyte alkaline phosphatase activity in rats exposed to vapors of various organic solvents.

Female Wistar rats were exposed to various solvent vapors 8 h/d for 7 d. The leukocyte suspension and serum were prepared from peripheral blood and utilized for the determination of alkaline phosphatase (AP) activity with disodium phenyl phosphate as a substrate [leukocyte AP (LAP) and serum AP (SAP) assay]. While the exposure to benzene at 20 or 50 ppm did not cause significant changes in LAP activity, the exposure at 100 and 300 ppm resulted in a dose-dependent increase of LAP activity up to more than 100% over the control. No further increase was observed at 1000 or 3000 ppm. Similar exposure at 300 ppm to either toluene, m-xylene, n-hexane, trichloroethylene, methyl ethyl ketone, ethyl acetate, or methyl alcohol did not induce any changes in LAP activity. Thus, the increase in LAP activity was considered to be specific to benzene exposure. When the animals were exposed to toluene (300 ppm) in combination with benzene (300 ppm), not only was the benzene-induced leukopenia alleviated as previously reported, but the benzene-induced increase in LAP activity was no longer observed. The parallel inhibitory effects of toluene on benzene-induced increase in LAP and leukopenia suggest that a relation may exist between increase in LAP activity and leukopenia. No changes in SAP activities were observed in the rats under the exposure conditions examined.

Effect of Timing of Cysteamine Administration on Duodenal Alkaline Phosphatase Activity in Rats with Restricted Two-Hour Feeding-Period

Effect of a restricted 2-h daily feeding period on the ulcerogenicity of cysteamine was studied in rats with special reference to duodenal alkaline phosphatase activity.Cysteamine was injected at 14:00, 16:00, 18:00, 20:00, or 23:00 to respective groups of rats fed a meal from 17:00-19:00 for 15 days. Twenty-four hours after each injection, duodenal alkaline phosphatase activity was measured in mucosal homogenates. In control rats given saline, an anticipated increase was observed in duodenal alkaline phosphatase activity at 1h before the meal, whereas cysteamine had a decreasing effect on the enzyme activity, which was most prominent when the drug was injected at 1h before the meal.

Change in alkaline phosphatase activity in rats administered cadmium chloride.

When cadmium (CdCl2) was administered subcutaneously in a high single dose of 5.0 mg/kg to rats, their liver and testis tissues showed a statistically significant increase in alkaline phosphatase (Al-P) activity at 24 h or more after the administration while the reverse was the case in the serum of the rats. Lactate dehydrogenase (LDH) activity in the serum showed a statistically significant decrease at 15 to 24 h after the administration of CdCl2. An increase in LDH activity for the serum coincided with that for the testis. During the study period there was no change in the calcium level in the serum, but the level of zinc in the serum decreased in a similar fashion to serum Al-P activity. As for the level of cadmium in the serum, it showed a very high value (ca. 0.03 mM) at 15 and 24 h after CdCl2 administration. When this concentration of cadmium was added in the form of CdCl2 to rat serum in vitro, it produced an inhibitory effect on serum Al-P activity. These facts suggest that the decrease in serum Al-P activity is not due to a change in tissue levels of Al-P, but reflects a direct inhibition of Al-P activity in the serum by cadmium.