## Background: The Harderian gland (HG) is a tubulo-alveolar gland found within the ocular orbit of animals which present a nictitating membrane. The Harderian gland is regarded as an extrapineal melatonin producing organ and both, photoperiod and melatonin have been shown to exert an important ro
Effects of the circadian mutation ‘tau’ on the Harderian glands of Syrian hamsters
✍ Scribed by Ana Coto-Montes; Cristina Tomás-Zapico; María Josefa Rodríguez-Colunga; Delio Tolivia-Cadrecha; Jorge Martínez-Fraga; Rüdiger Hardeland; Delio Tolivia
- Publisher
- John Wiley and Sons
- Year
- 2001
- Tongue
- English
- Weight
- 348 KB
- Volume
- 83
- Category
- Article
- ISSN
- 0730-2312
- DOI
- 10.1002/jcb.1240
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✦ Synopsis
Abstract
The Syrian hamster Harderian gland (HG) is an organ continually exposed to oxidative stress caused by high concentrations of porphyric metabolites. According to previous studies, melatonin, which is rhythmically secreted by the pineal gland and tonically produced by the HG, antagonizes the oxidative damage. HGs exhibit a strong gender‐dependent correlation between porphyrins, melatonin, and histological appearance. In HGs of both sexes, we have investigated effects of a single gene defect in the circadian clock system (tau mutation) causing a shortened free‐running period and an advanced maximum of circulating melatonin. Comparisons were made with wild‐type animals, one group of which received daily pharmacological injections of melatonin in late photophase. Changes were observed in histological characteristics, porphyrin content, antioxidant enzyme activities, and damage of proteins and lipids. HGs of tau hamsters showed morphological changes which can be partially interpreted in terms of increased damage. Additionally, tau females exhibited a many‐fold augmentation in the percentage of so‐called type II cells, which are otherwise typical for the male glands. In tau hamsters of both sexes, major antioxidative enzyme activities (superoxide dismutase, glutathione reductase, and catalase) were markedly enhanced, a presumably compensatory response to increased oxidative stress. Higher oxidative damage in tau HGs was directly demonstrable by a many‐fold increase in protein carbonyl. Rises in antioxidative enzymes were also observed upon injections of melatonin; this was, however, not accompanied by changes in protein carbonyl, so that enzyme inductions by the hormone should be understood as protective actions. Our data are not only in accordance with findings on protective effects by melatonin, but also with our earlier observation made in Drosophila that perturbations in the circadian system lead to increased oxidative stress. J. Cell. Biochem. 83: 426–434, 2001. © 2001 Wiley‐Liss, Inc.
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