acid-phosphatase and Lead-Poisoning

The major portion of lead in the body resides in skeletal system. The bone turnover affects the release of lead into the circulation from bones. The bone turnover biomarkers (BTM) in lead-battery workers with long-term exposure to lead have not been explored yet.. To evaluate the BTM (formation and resorption) in lead-battery workers with long-term exposure to lead in lead-battery manufacturing plant.. 176 male lead-exposed workers and 80 matched comparison group were studied. All participants were examined for blood lead levels (BLLs), bone formation biomarkers- serum osteocalcin (OC), alkaline phosphatase (ALP), bone-specific alkaline phosphatase (BALP)-and bone resorption biomarkers-serum pyridinoline (PYD), deoxypyridinoline (DPYD), tartarate-resistant acid phosphatase-5b (TRACP-5b), and urinary hydroxyproline (UHYP).. We found a significantly higher bone formation biomarkers such as BALP (p=0.007) and bone resorption biomarkers, eg, PYD (p=0.048), TRCAP-5b (p=0.001), and UHYP (p=0.001) in lead-exposed workers. A significant (p=0.041) negative correlation (ρ ‑0.128) was noted between BLLs and OC. A significant positive correlation was noted between BLLs and TRACP-5b (ρ 0.176, p=0.005) and UHYP (ρ 0.258, p=0.004). Serum OC (p=0.040) and UHYP (p=0.015) levels changed significantly with BLL level. Bone resorption biomarkers levels- PYD, TRACP-5b, and BALP-were higher among those with higher BLLs levels. The duration of exposure was significantly associated with BALP (p=0.037), DPYD (p=0.016), TRACP-5b (p=0.001), and UHYP (p=0.002) levels.. Long-term lead exposure affects the bone turnover.

Topics: Acid Phosphatase; Adult; Alkaline Phosphatase; Biomarkers; Bone Remodeling; Bone Resorption; Case-Control Studies; Cross-Sectional Studies; Electric Power Supplies; Humans; Isoenzymes; Lead; Lead Poisoning; Male; Manufacturing and Industrial Facilities; Middle Aged; Occupational Exposure; Osteocalcin; Workplace

The toxic effect of Pb ion (lead acetate) was investigated using male albino rats, which was ingested at 1/20, 1/40, and 1/60 sublethal doses. Relative to normal control, the ingestion of Pb(2+) induced significant stimulation in ALT and AST activity. In addition, total soluble protein and albumin contents of plasma were decreased, while the content of globulin was changed by the Pb(2+) treatments. The cholinesterase activity was inhibited, but the activities of alkaline and acid phosphates as well as lactate dehydrogenase were stimulated as a result of lead acetate intoxication. These observations were gradually paralleled across the experiment dose of the three doses of intoxicated Pb(2+). In the case of blood picture, Pb(2+) ingestion significantly reduced the contents of hemoglobin and RBC count of intoxicated rat's blood, while the plasma levels of T3 and T4 and blood WBC count were insignificantly decreased or unchanged. All results of the present study showed that the Pb(2+) ingestion was more effective in the case of the high dose (1/20 LD(50)) than that of the low dose (1/60 LD(50)) ingestion relative to the normal healthy control. The results of the present work advice the need to avoid exposure of humans to the lead compound to avoid injurious hazard risk.

Topics: Acid Phosphatase; Alkaline Phosphatase; Animals; Blood Cell Count; Blood Chemical Analysis; Blood Proteins; Body Weight; Cholinesterases; Eating; Kidney Function Tests; Lead Poisoning; Lethal Dose 50; Liver Function Tests; Male; Organometallic Compounds; Rats; Rats, Sprague-Dawley; Thyroid Gland; Weight Gain

Lead acetate (300 mg Pb/L) and/or cadmium acetate (10mg Cd/L) in blood and liver were administrated as drinking water to pregnant Wistar rats from day 1 of pregnancy to parturition (day 0) or until weaning (day 21), to investigate the toxic effects in blood and in the liver. Both metals produced mycrocitic anaemia in the pups as well as oxidative damage in the liver, as suggested by the significant increase in TBARS production and the high catalase activity. Moreover, intense alkaline and acid phosphatase activity, used as biomarkers of liver adaptation to damaging factors, was observed. In addition, the toxikinetics are different for Pb and Cd: while Cd is a hepatotoxic from day 0, Pb is not until day 21. Finally, simultaneous perinatal administration of both metals seems to protect, at least, in the liver TBARS production against the toxicity produced by Cd or Pb separately.

Topics: Acid Phosphatase; Alkaline Phosphatase; Animals; Animals, Newborn; Cadmium; Cadmium Poisoning; Catalase; Chemical and Drug Induced Liver Injury; Drug Combinations; Female; Lead; Lead Poisoning; Liver Diseases; Organ Size; Oxidative Stress; Pregnancy; Rats; Rats, Wistar; Thiobarbituric Acid Reactive Substances

Administration of 0.01 and 0.1 mg of lead nitrate for 4 and 7 days and infection of Ancylostoma caninum larvae orally altered the activation of alkaline phosphatase and acid phosphatase in the hearts of mice when compared to infected animals and controls. Alkaline phosphatase activity increased significantly in all drug-treated + infected mice. The level of acid phosphatase decreased significantly in mice exposed to chronic doses of lead. The altered levels of alkaline phosphatase and acid phosphatase suggest that administration of lead could cause toxicity in the heart, disturbing the cellular metabolism; infection alone could not cause any significant changes in enzymes of heart.

Topics: Acid Phosphatase; Alkaline Phosphatase; Ancylostoma; Ancylostomiasis; Animals; Disease Models, Animal; Female; Lead Poisoning; Mice; Myocardium

Seven hepatic phosphatases were histochemically investigated in male white rats (Rattus norvegicus) pretreated with chronic subtoxic doses of lead acetate. Lead has increased the activities of alkaline-, acid-, neutral-, adenosine mono- and glucose-6-phosphatase, but has markedly decreased the activity of membrane-bound Na+-K+, ATPase while the activity of mitochondrial Mg2+-ATPase was not altered. It has also produced heterogenous alterations in the distribution patterns, sites of the enzymatic activities and in the intensity of phosphatase activities among the same type of cells in the terminal afferent and efferent venules of the hepatic lobules. The obtained histochemical findings indicate that the alterations in the activities of hepatic phosphatases could be an adaptation to the metabolic, structural and functional changes in the organelles of hepatic cells due to lead intoxication.

Topics: Acid Phosphatase; Alkaline Phosphatase; Animals; Histocytochemistry; Lead; Lead Poisoning; Liver; Male; Mitochondria, Liver; Nucleotidases; Organometallic Compounds; Phosphoric Monoester Hydrolases; Rats; Rats, Wistar; Sodium-Potassium-Exchanging ATPase

Male albino rats were intramuscularly administered a single dose of lead acetate (100 micromol/kg b.wt). Another group of rats were injected with sodium selenite (10 micromol/kg b.wt) before lead intoxication. After 3 and 24 hours, lead treatment resulted in significant increases in acid and alkaline phosphatases, GOT and GPT, total proteins, and cholesterol in serum. The total triglycerides in serum was decreased after 24 hours of intoxication. Lead treatment also produced significant elevation of lipid peroxidation in liver and kidney. The antioxidant capacity of hepatic and renal cells in terms of the activities of superoxide dismutase, glutathione reductase, and glutathione content was diminished. It appears from these results that lead may exert its toxic effect via peroxidative damage to renal and hepatic cell membranes after 24 hours. Selenium administration prior to lead injection produced pronounced prophylactic action against lead effects, and it is observed that selenium enhances the endogenous antioxidant capacity of the cells by increasing the activities of the superoxide dismutase and glutathione reductase and the glutathione content. As a result, the lipid peroxidation was decreased in both liver and kidney.

Topics: Acid Phosphatase; Alanine Transaminase; Alkaline Phosphatase; Animals; Aspartate Aminotransferases; Glutathione; Kidney; Lead Poisoning; Lipid Peroxidation; Liver; Male; Organometallic Compounds; Rats; Selenium; Superoxide Dismutase

An investigation on the influence of lead toxicity on some of the hepatic enzymes was studied in rats both after a shorter interval of 15 d and after longer intervals of 60 and 90 d. Three different doses of lead as 5, 10, and 50 mg/kg body wt were administered orally on every alternate day. Whereas significant inhibition of succinic dehydrogenase was seen following lead poisoning, the activity acid and alkaline phosphatase increased with lead intoxication. The histoarchitecture of the liver was grossly intact. Liver accumulated less lead compared to kidney at 60 and 90 d.

Topics: Acid Phosphatase; Alkaline Phosphatase; Animals; Female; Kidney; Lead; Lead Poisoning; Liver; Rats; Spectrophotometry, Atomic; Succinate Dehydrogenase; Time Factors

Topics: Acetylcholinesterase; Acid Phosphatase; Alanine Transaminase; Alkaline Phosphatase; Animals; Aspartate Aminotransferases; Energy Metabolism; Enzymes; Fishes; L-Lactate Dehydrogenase; Lead Poisoning; Synaptic Transmission

The purpose of the study was assessment of the effect of an environment contaminated with heavy metals on the activity of certain enzymes of mixed saliva. The activity was determined of total acid phosphatase and phosphatase resistant to tartrate and formaldehyde, alkaline phosphatase, alanine and aspartate aminotransferase, and alpha-amylase. The studied material comprised 110 saliva samples obtained from three groups of children aged 8 years. Group I of 21 children lived in Szopienice, group II of 30 children lived in Miasteczko Slaskie. In both these localities the children were exposed to mean daily concentrations, above the permitted ones, mainly of lead compounds, in lower degree to cadmium and zinc compounds. Environment contamination in Szopienice was greater than in Miasteczko Slaskie. Group III of 59 children living in Lubowice served as controls. In that town the permissible concentrations of these compounds were not exceeded. Statistical analysis of these results showed that the activity of total acid phosphatase in groups I and II, that is in the contaminated areas, was highly significantly greater than in the control group. The activity of alkaline phosphatase was raised only in the saliva in group I. No differences were found in the activity of alpha-amylase and aminotransferases.

Topics: Acid Phosphatase; Alanine Transaminase; Alkaline Phosphatase; alpha-Amylases; Aspartate Aminotransferases; Cadmium Poisoning; Child; Environmental Exposure; Female; Humans; Lead Poisoning; Male; Maximum Allowable Concentration; Saliva; Zinc

Topics: Acid Phosphatase; Acute Disease; Animals; Chronic Disease; Histocytochemistry; L-Lactate Dehydrogenase; Lead Poisoning; Lipid Metabolism; Liver; Liver Glycogen; Male; Rats; Succinate Dehydrogenase

Topics: Acid Phosphatase; Alkaline Phosphatase; Animals; Aspartate Aminotransferases; Copper; Enzymes; Female; gamma-Glutamyltransferase; L-Lactate Dehydrogenase; Lead Poisoning; Male; Penicillamine; Rats; Zinc

The effect of LC(50) and a sublethal concentration of lead nitrate on the activities of alkaline phosphatase, acid phosphatase, glucose-6-phosphatase, lipase and urease in the kidneys and ovaries of a teleost fish, Channa punctatus has been examined after 96 hr and 30 days respectively. The results show that all the five enzymes in the two tissues are inhibited significantly at both the experimental stages. However, the inhibition produced after 30 days by the sublethal concentration ish higher indicating the cumulative action of lead. Further, the inhibition of enzymes is, more marked in kidney than in the ovary.

Topics: Acid Phosphatase; Alkaline Phosphatase; Animals; Female; Fishes; Glucose-6-Phosphatase; Kidney; Lead; Lead Poisoning; Lipase; Nitrates; Ovary; Urease

The effect of acute and repeated action of cobalt, lead, antimony on the metabolism of the heart muscle is shown. High doses of the metals of approximately 1/5 LD50 were studied in the acute experiment and doses one fifth these in the repeated experiment. The data obtained indicated that due to the effect of all the poisons studied changes developed early in catecholamine metabolism - the myocardial noradrenaline content decreased and the blood and urine monamine levels rose. Increase in the content of pyruvic acid, intensification of glycogenolysis processes (increase in phosphorylase a activity and decrease in the glycogen level), and diminished activity of lactate dehydrogenase in the myocardium attested to changes in its metabolism. High doses of the metals caused an increase in the free activity of the lysosome enzymes, cathepsins and of acid phosphatase, which indicated that the permeability of the membranes of these organelles was disturbed. The mechanism of the cardiotoxic effect of the metals is discussed.

Topics: Acid Phosphatase; Animals; Antimony; Catecholamines; Cathepsins; Cobalt; Heart Diseases; L-Lactate Dehydrogenase; Lead Poisoning; Lysosomes; Male; Myocardium; Phosphorylases; Rats

Topics: Acid Phosphatase; Alkaline Phosphatase; Animals; Esterases; Histocytochemistry; Kidney; Lead Poisoning; Nucleotidases; Sciuridae

Topics: Acid Phosphatase; Alanine Transaminase; Alkaline Phosphatase; Animals; Aspartate Aminotransferases; Cell Survival; Cysteine; Glucuronidase; Kupffer Cells; Lactates; Lead Poisoning; Liver; Male; Methylprednisolone; Phagocytosis; Pyruvates; Rats; Salmonella enteritidis; Shock, Septic; Sulfobromophthalein

Topics: Acid Phosphatase; Animals; Animals, Newborn; Body Weight; Carbon Isotopes; Cathepsins; Cell Membrane; Cytosine Nucleotides; Glucosidases; Glycoproteins; Hydrolases; Kidney; Lead Poisoning; Neuraminic Acids; Neuraminidase; Nucleotidyltransferases; Organ Size; Peptide Hydrolases; Proteins; Rats; Transferases

Topics: Acid Phosphatase; Animals; Cells, Cultured; Cytoplasmic Granules; Embryo, Mammalian; Female; Fibroblasts; Histocytochemistry; Lead; Lead Poisoning; Lysosomes; Membranes; Pregnancy; Rats; Silver; Sulfides

Topics: Acetylcholinesterase; Acid Phosphatase; Amino Acids; Animals; Enzymes; Erythrocytes; Glucosephosphate Dehydrogenase; Glycolysis; Hexosephosphates; Lead; Lead Poisoning; Levulinic Acids; Malate Dehydrogenase; Methemoglobin; Oxidoreductases; Rabbits

Topics: Acid Phosphatase; Alcohol Oxidoreductases; Animals; Aspartate Aminotransferases; Cytoplasm; Erythrocytes; Glutamate Dehydrogenase; Guinea Pigs; Isoenzymes; L-Lactate Dehydrogenase; Lead Poisoning; Liver; Lysosomes; Male; Ribonucleases; Sorbitol

Topics: Acid Phosphatase; Adenosine Triphosphatases; Alanine Transaminase; Alkaline Phosphatase; Animals; Benzene; Cell Membrane; Drug Synergism; Electrocardiography; Heart; Histocytochemistry; Hydrocarbons; Lead Poisoning; Myocardium; Nucleotidases; Organometallic Compounds; Rabbits; Succinate Dehydrogenase

Topics: Acid Phosphatase; Adenosine Triphosphate; Animals; Cell Membrane; Cell Wall; Gingiva; Histocytochemistry; Lead Poisoning; Mouth Mucosa; Rabbits; Salivary Glands

Topics: Acid Phosphatase; Aerosols; Animals; Canaries; Chickens; Cilia; Common Cold; Disease; Environmental Exposure; Epithelium; Humans; Humidity; Lead Poisoning; Malaria; Mice; Mucous Membrane; Newcastle disease virus; Orthomyxoviridae; Parathion; Pneumonia; Rats; Respiratory Tract Infections; Skin Diseases; Temperature

Topics: Acid Phosphatase; Animals; Chronic Disease; Histocytochemistry; Lead Poisoning; Nerve Degeneration; Peripheral Nerves; Rats

Topics: Acid Phosphatase; Alkaline Phosphatase; Animals; Brain; Histocytochemistry; Lead Poisoning; Rats

Topics: Acid Phosphatase; Adenosine Triphosphatases; Alkaline Phosphatase; Animals; Histocytochemistry; Intestines; Kidney; Lead Poisoning; Liver; Rabbits

Topics: Acid Phosphatase; Adenosine Triphosphatases; Alkaline Phosphatase; Animals; Dihydrolipoamide Dehydrogenase; Female; Gingiva; Lead Poisoning; Mouth Mucosa; Rabbits; Salivary Glands

Topics: Acid Phosphatase; Adenosine Triphosphatases; Alkaline Phosphatase; Animals; Lead Poisoning; Muscle, Striated; Muscles; Myocardium; Phosphoric Monoester Hydrolases; Rabbits; Research; Toxicology

Topics: Acid Phosphatase; Brain; Humans; Lead Poisoning; Neurochemistry; Poisoning; Tetraethyl Lead