Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Injections, Intraperitoneal”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 73 records · Page 4Linked to original sources
PubMed1993

Neurotoxicity of glycidamide, an acrylamide metabolite, following intraperitoneal injections in rats.

Acrylamide (2-propenamide) monomer produces central-peripheral distal axonopathy in humans and some animal species. Its neurotoxicity is characterized by abnormal sensation, decreased motor strength, and ataxia. Acrylamide forms adducts with glutathione, proteins, and DNA. Recent studies demonstrated that acrylamide is metabolized to its epoxide, glycidamide (2,3-epoxy-1-propanamide). We studied the neurotoxicity potential of glycidamide in male Sprague-Dawley rats. Animals (groups of 6) were injected ip daily with either aqueous acrylamide or glycidamide at an acrylamide-equivalent dose of 50 mg/kg (0.70 mmol/kg). Both treatments resulted initially in the rats circling, which was followed by the onset of ataxia at 7-9 d and hindlimb paralysis at 12-14 d. Treated animals showed muscle wasting. At termination, acrylamide- and glycidamide-treated rats weighed 105% and 86% of initial weight, respectively, compared to 145% for controls. Animals were anesthetized and perfused with 10% neutral phosphate-buffered formalin 12 or 14 d after beginning of treatment. Both treatment groups exhibited similar neuropathologic changes in the central and peripheral nervous systems. More severe lesions were produced by glycidamide. A marked increase in the number of affected Purkinje cells in the cerebellum, which exhibited changes ranging from pyknosis to cell death, were present. The brainstem exhibited axonal degeneration with chromatolytic necrosis in midbrain medial and lateral reticular nuclei. The spinal cord was characterized by spongy form changes with vacuoles of different sizes in various levels. These results suggest that glycidamide is an active neurotoxic metabolite of acrylamide.

Acrylamide↗
PubMed1979

Acrylic microspheres in vivo. I. Distribution and elimination of polyacrylamide microparticles after intravenous and intraperitoneal injection in mouse and rat.

Microspheres of 14C-labeled highly cross-linked polyacrylamide (mean diameter 0.25-0.30 micron) have been prepared by emulsion polymerization. The label was introduced in the polymer via the cross-linking monomer. N,N'-[14C]methylenebisacrylamide. The microparticles were used to follow qualitatively and quantitatively the distribution and the fate of polyacrylamide in mouse and rat after i.v. and i.p. injection. The polyacrylamide particles are rapidly cleared from the circulation (t 1/2 in rat approximately 40 min) by macrophages of the reticuloendothelial system. They are mainly (about 80%) found in the liver and spleen both after i.v. and i.p. injection (4.1 mg given totally to mice weighing 20-25 g). They can also be detected early (1 hr after i.v. injection) in the bone marrow, and particle aggregates are also initially found in the lungs, although no respiratory problems were noted. After about 16 weeks, the radioactivity rapidly decreases in the liver and spleen, with t 1/2 10 to 14 weeks and 15 to 24 weeks, respectively, depending on the route of administration. Radioactivity in the gut and gut walls detected 2 months after injection suggests that the polyacrylamide is slowly metabolized. No toxic effects-apart from transient hepatospleenomegaly-were detected in mice 45 weeks after they were given a total of 9.8 mg of polyacrylamide.

Acrylamides↗
PubMed1985

[Binding of 3H-spiperone in the mouse brain after intraperitoneal injection].

In experiments on mice 3H-spiperone binding after intraperitoneal injection was studied. The binding of 3H-spiperone was saturable in the frontal cortex and subcortical structures, whereas in the cerebellum, the amount of radioactivity increased in a linear manner and was referred to as nonspecific binding. The neuroleptics haloperidol, chlorpromazine and sulpiride given 0.5 h before 3H-spiperone displaced 3H-spiperone in the subcortical structures in a dose-related manner. Although the level of the specific 3H-spiperone binding after intraperitoneal injection was lower than after intravenous injection, the intraperitoneal method is simpler, well reproduced and given results comparable with the intravenous method.

Animals↗