acid-phosphatase and Paralysis

A severely osteopenic rat model was obtained by combining orchidectomy (ORX) and disuse (due to local paralysis induced by botulinum toxin [BTX] in the quadriceps muscle).. Forty-two aged male rats (5-6 months old) were randomized into three groups: 18 were SHAM operated; 6 were ORX; and 18 were ORX and BTX injected in the right hindlimb. One, two, and three months after surgery, bone mass (BV/TV) and microarchitectural parameters (Tb.Th, Tb.N, Tb.Sp, Tb.Pf, and structure model index [SMI]) were measured by microcomputed tomography (microCT) on the primary and secondary spongiosa of the femur. Osteoid parameters (OS/BS, O.Th), the number of osteoclasts (Nb.Oc), and the mineral apposition rate (Ct.MAR, Cn.MAR) were measured by histology. The serum tartrate-resistant acid phosphatase (TRAcP) 5b activity was measured by immunoassay.. ORX induced a decrease of BV/TV, Tb.N and an increase of Tb.Sp, Tb.Pf, and SMI on both primary and secondary spongiosa. ORX and BTX had cumulative effects on bone loss, since differences were maximized on the right femur. The decrease in BV/TV reached -65%. Osteoid parameters and mineral apposition rate increased during the time course of the study. A peak of serum TRAcP was found at 7 days post-ORX. TRAcP levels reached the highest values in the ORX-BTX groups and the effect lasted longer than in the group with ORX alone. The association of ORX-BTX induced a greater bone resorption, due to the removal of complete trabeculae, compared to ORX alone.. This model induced a severe and rapid bone loss and can be used to explore pharmacological- and biomaterial-based countermeasures.

Topics: Acid Phosphatase; Animals; Botulinum Toxins; Disease Models, Animal; Imaging, Three-Dimensional; Isoenzymes; Male; Orchiectomy; Osteoclasts; Osteoporosis; Paralysis; Rats; Rats, Wistar; Tartrate-Resistant Acid Phosphatase; Tomography, X-Ray Computed

Topics: Acid Phosphatase; Animals; Aspartic Acid Endopeptidases; beta-Galactosidase; Chickens; Endopeptidases; Enzyme Activation; Female; Lysosomes; Organophosphorus Compounds; Paralysis; Rats; Sciatic Nerve; Spinal Cord

The changes in brain acetylcholinesterase (AChE), acid phosphatase (APase), and 2',3'-cyclic nucleotide-3'-phosphohydrolase (CNP), and plasma butyrylcholinesterase (BuChE) activities were investigated in hens treated with a single, dermal dose (100-1000 mg/kg) of S,S,S-tri-n-butyl phosphorotrithioate (DEF). Three control groups consisted of hens left untreated, given a single, dermal dose of 500 mg/kg tri-o-cresyl phosphate (TOCP, positive control for organophophorous compound-induced delayed neurotoxicity), or 10 mg/kg O,O-diethyl O-4-nitrophenyl phosphorothioate (parathion, negative control). Brain AChE activity, determined 28 days after application, was significantly inhibited in hens given 500-1,000 mg/kg DEF and in TOCP- and parathion-treated hens. In contrast, brain APase and CNP activities were significantly higher in all treatments as compared with those of the untreated hens. Parathion, however, caused the least increase in these enzymatic activities as compared to DEF or TOCP. A single, dermal dose of DEF or TOCP also caused an initial decrease in plasma BuChE activity with maximum depression of enzymatic activity observed 1 to 7 days after administration. This decrease was dose dependent and the enzymatic activity showed partial recovery with time. Hens treated with single, dermal doses of DEF, ranging from 250 to 1000 mg/kg, developed ataxia which progressed to paralysis in some hens. Histopathologic examination revealed axon and myelin degeneration of the spinal cord and peripheral nerves of some hens. The severity and frequency of the neuropathologic lesions were dose dependent. Neurologic dysfunctions and neuropathologic lesions seen in DEF-treated hens were similar to those exhibited in TOCP-treated hens. While parathion produced acute cholinergic effects, it did not cause delayed neurotoxicity. The changes in brain and plasma enzymes are discussed in relation to their role in the pathogenesis of DEF-induced delayed neurotoxicity.

Topics: Acetylcholinesterase; Acid Phosphatase; Administration, Topical; Animals; Ataxia; Body Weight; Brain; Butyrylcholinesterase; Chickens; Cholinesterases; Female; Organothiophosphates; Organothiophosphorus Compounds; Paralysis; Parathion; Peripheral Nerves; Spinal Cord; Tritolyl Phosphates

Topics: Abdominal Neoplasms; Acid Phosphatase; Acute Disease; Aminosalicylic Acid; B-Lymphocytes; Child; Diagnosis, Differential; Humans; Leukemia; Leukemia, Lymphoid; Leukemia, Myeloid, Acute; Leukocytes; Mediastinal Neoplasms; Osteomyelitis; Paralysis; Rheumatic Diseases; Sepsis; T-Lymphocytes

The effect of feeding stable strontium (Sr) on the tissue alkaline and acid phosphatase activities was studied in young rats. These activities were reduced in liver and small intestine by 10% to 15% at 2 weeks, 20% to 30% at 4 weeks and in kidney by 20% at 6 weeks only in rats fed 2% Sr diet; bone alkaliine phosphatase activity was, however, increased by 80% to 100% (2-6 weeks) in these rats. Gross lesions like paralysis, hemorrhage, rickets and high mortality were observed after 4 to 6 weeks. Although no such lesions were seen, appreciable changes in enzyme activities as mentioned above were discernible in rats fed 1% Sr diet for 6 weeks. Feeding of a 0.5% Sr diet for a period up to 6 weeks had no deleterious effect. Recovery following consumption of a normal diet for 2 weeks was almost complete in liver and small intestine but not in kidney. The elevated tissue Sr levels do not explain the pronounced losses seen in this investigation as compared to those in the earlier in vitro experiments. This study depicts the possible damage due to prolonged therapeutic use of large amounts of stable Sr for the removal of radiostrontium.

Topics: Acid Phosphatase; Alkaline Phosphatase; Animals; Body Weight; Bone and Bones; Dose-Response Relationship, Drug; Hemorrhage; Intestine, Small; Kidney; Liver; Male; Paralysis; Rats; Strontium

Topics: Acid Phosphatase; Adenosine Triphosphatases; Alkaline Phosphatase; Animals; Basal Ganglia; Brain; Caudate Nucleus; Cerebral Cortex; Hindlimb; Histocytochemistry; Male; Manganese Poisoning; Nerve Degeneration; Neuroglia; Neurons; Nucleotidases; Paralysis; Rabbits; Substantia Nigra; Time Factors

Topics: Acid Phosphatase; Adolescent; Adult; Blood Group Antigens; Child; Child, Preschool; Creatine Kinase; Dihydrolipoamide Dehydrogenase; Female; Haptoglobins; Histocytochemistry; Humans; Hyperkalemia; Immunoglobulins; Male; Middle Aged; Muscles; Myotonia Congenita; Paralysis; Pedigree; Phosphoglucomutase; Phosphogluconate Dehydrogenase; Phosphotransferases; Potassium; Transferrin

Topics: Acid Phosphatase; Adenocarcinoma; Cranial Nerves; Humans; Male; Middle Aged; Neoplasm Metastasis; Paralysis; Prostatic Neoplasms; Skull Neoplasms; Tomography; Vocal Cord Paralysis

Topics: Acid Phosphatase; Animals; Chickens; Cytoplasm; Diphtheria Antitoxin; Diphtheria Toxin; Electrons; Lysosomes; Microscopy; Microscopy, Electron; Myelin Sheath; Paralysis; Pathology; Pharmacology; Poultry; Research; Schwann Cells; Toxicology