Histamine and histamine-5 Gy groups received a daily subcutaneous histamine injection (0.1 mg/kg) starting 24 h before irradiation. Histamine-5 Gy and untreated-5 Gy groups were irradiated with a single dose of whole-body Cesium-137 irradiation. Control and untreated-5 Gy groups were given daily saline injections. Three days post irradiation metacholine-induced salivary secretion was measured or animals were sacrificed and submandibular gland (SMG) removed, stained and histological characteristics were evaluated. Proliferation and apoptosis markers were studied by immunohistochemistry.

Results:

MAPK Inhibitor Library Radiation decreased salivary secretion by 40% in comparison to untreated rats, which was associated with loss of SMG mass, alteration of epithelial architecture,

partial loss of secretor granular material, diminished proliferation and a remarkable apoptotic response. In contrast, histamine completely reversed the reduced salivation induced by radiation, conserved glandular mass with normal appearance and preserved GSK621 datasheet the structural organisation of secretor granules. Radiation-induced toxicity is prevented by histamine essentially by suppressing apoptosis of ductal and acinar cells, reducing the number of apoptotic cells per field (19.0 +/- 3.8 vs. 106.0 +/- 12.0 in untreated animals, P < 0.001), and also by preventing the radiation-induced decrease in cell proliferation.

Conclusions: Histamine prevents morphological and functional radiation-induced damage on SMG, representing a potential radioprotector for treatment of patients undergoing radiotherapy for head and neck malignancies.”
“Aim: Whether arteries are affected in mitochondrial disorders (MIDs) was under debate for years but meanwhile there MAPK inhibitor are strong indications that large and small arteries are primarily or secondarily affected in MIDs.

Data synthesis: When reviewing the literature for appropriate studies it turned out that vascular involvement in MIDs includes primary or secondary micro- or macroangiopathy of the cerebral, cervical, and retinal arteries, the aorta, the iliac arteries, the brachial arteries, or the muscular arteries. Arteriopathy

in MIDs manifests as atherosclerosis, stenosis, occlusion, dissection, ectasia, aneurysm formation, or arteriovenous malformation. Direct evidence for primary cerebral microangiopathy comes from histological studies and indirect evidence from imaging and perfusion studies of the brain. Microangiopathy of the retina is highly prevalent in Leber’s hereditary optic neuropathy. Macroangiopathy of the carotid arteries may be complicated by stroke. Arteriopathy of the aorta may result in ectasia, aneurysm formation, or even rupture. Further evidence for arteriopathy in MIDs comes from the frequent association of migraine with MIDs and the occurrence of premature atherosclerosis in MID patients without classical risk factors.