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Biomedical subjects

I Mahmoud

Publications and source records attributed to I Mahmoud.

2 recordsLinked to original sources

Continuous darkness and continuous light induce structural changes in the rat thymus.

It is known that neuroendocrine responses to environmental stimuli, such as light, can influence immune responses through the pineal gland. It is also known that periods of constant darkness and constant light cause stimulation and inhibition of melatonin secretion from the pineal gland, successively. In this study, we provide experimental evidence that changes in the rhythm of the photoperiod have considerable effects on thymic structure of the rat. Male albino Wistar rats were divided into 3 groups. Group 1 rats were kept in a dark room, group 2 in a room under a bright artificial light and group 3 (control) animals were exposed to a 12:12 h light: dark cycle. All animals were killed after 4 wk. In group 1, thymus weight increased by 315%, the increase in volume affecting the medulla (cortex 190%, medulla 655%). The absolute number of epithelial cells and lymphocytes increased both in the cortex and medulla. Thymic cortical epithelial cells were hypertrophied and contained numerous large clear vesicles. Perivascular spaces were enlarged. In group 2 thymus weight decreased by 53%, the reduction in volume affecting mainly the cortex (cortex 61%, medulla 27%). The absolute numbers of cortical epithelial cells and lymphocytes were decreased, and pyknotic lymphocyte nuclei were frequent both in the cortex and medulla. It is concluded that constant darkness causes hypertrophy and increased cellularity of the thymus, while constant light causes involution of the thymus and death of lymphocytes. These changes possibly reflect the well known immunostimulatory effects of melatonin acting directly or indirectly, on the thymic lymphocytes and epithelial cells.

Animals

Direct toxic effect of iodide in excess on iodine-deficient thyroid glands: epithelial necrosis and inflammation associated with lipofuscin accumulation.

Involution of thyroid hyperplasia (induced by a low iodine diet and a goitrogen, propylthiouracil, PTU) was obtained in mice by administering a high or a moderate dose of iodide (HID or MID, respectively). In HID involuting glands, vasoconstriction was observed after 12 hr whereas necrosis and inflammation were very abundant as early as after 6 hr and maximal after 48 hr. They were not prevented by papaverine by which vasoconstriction was inhibited, but were inhibited by the continuation of PTU by which iodide oxidation and organification were inhibited. Lipofuscin inclusions in thyroid and inflammatory cells were always associated with necrosis. On the contrary, when involution was induced by MID or by HID + triiodothyronine (T3), or by T3 alone, neither necrosis nor inflammation occurred and apoptosis was the only mode of cell deletion. No lipofuscin inclusion occurred. Our results demonstrate that iodide in excess, after being oxidized or organified, is directly toxic for iodine-deficient thyroid cells. The presence of lipofuscin suggests that its toxicity is mediated by lipid peroxidation, a consequence of production of free radicals in excess.

Animals