triethyltin-sulfate and Brain-Edema

This study examined the early response of pro-inflammatory and regulatory cytokines in the mouse brain following triethyltin (TET)-induced myelin injury characterized by edematous vacuolation. Following an acute intraperitoneal injection of triethyltin (TET) sulfate (3 mg/kg) to 17-day old CD1 mice, significant increases in brain stem TNF-alpha and IL-1alpha mRNA levels occurred at 6 and 24 h, respectively with elevations in TGF-beta1 and MIP-1alpha at 1 h. In the cortex, responses were limited to elevations at 6 h in TNF-alpha, TGF-beta1 and MIP-1alpha. These data suggest that a chemokine/cytokine response can occur with minimal alterations to the integrity of the myelin sheath and may contribute to the initial signaling mechanisms associated with demyelinating disorders.

Topics: Animals; Brain Edema; Brain Stem; Chemokine CCL3; Chemokine CCL4; Cytokines; In Situ Hybridization; Macrophage Inflammatory Proteins; Male; Mice; Mice, Inbred Strains; Microscopy, Electron; Myelin Sheath; Ribonucleases; RNA, Messenger; Transforming Growth Factor beta; Triethyltin Compounds

In golden hamsters, a study was made on the vascular permeability changes which might take place during the formation of triethyltin (TET)-induced brain edema. For this purpose, the animals received a single intravenous (i.v.) injection of TET sulphate (5-10 mg/kg b.wt) and groups of animals were studied 4 to 24 h thereafter. By the use of a new density gradient technique based on polyvinylcoated silica particles (1), it was shown that white matter edema was present already at 4 h after the TET injection. The edema then progressed during the following 20 h. Electron microscopy revealed that fluid accumulated in myelin vacuoles of the hamsters in the same way as has been described in other animal species. The macromolecular tracer, horseradish peroxidase mol.wt 40,000 injected i.v., did not leak out of the cerebral vessels during the period when edema developed. In order to find out if the formation of edema is associated with a vascular permeability increase to other and smaller markers, we used several fractions of FITC-dextrans varying from mol.wt 3,000 to 70,000 and determined their intracerebral localization with a histotechnical procedure. FITC-dextrans, mol.wt 70,000, did not leak out of the cerebral vessels in any of the TET intoxicated hamsters during the observation period of 24 h. The same was true for most animals given the other dextran fractions. However, FITC-dextrans, mol.wt 3,000-20,000 were present outside the vessels in the edematous optic nerves and corpus callosum in a few TET treated animals taken 16-24 h after the TET injection.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Animals; Blood-Brain Barrier; Brain Edema; Capillary Permeability; Cricetinae; Dextrans; Fluorescein; Fluorescein-5-isothiocyanate; Fluoresceins; Horseradish Peroxidase; Male; Microscopy, Electron; Microscopy, Fluorescence; Molecular Weight; Myelin Sheath; Specific Gravity; Trialkyltin Compounds; Triethyltin Compounds; Water-Electrolyte Balance

Topics: Animals; Brain Edema; Electrons; Hypertonic Solutions; Microscopy; Microscopy, Electron; Pathology; Pharmacology; Rabbits; Research; Sodium; Sulfates; Tin; Tin Compounds; Triethyltin Compounds; Urea