Coto-Montes Ana, Tomás-Zapico Cristina
Departamento de Morfología y Biología Celular, Facultad de Medicina, Universidad de Oviedo, Oviedo, Spain. acoto@@uniovi.es
Autophagy. 2006 Apr-Jun;2(2):126-8. doi: 10.4161/auto.2.2.2351. Epub 2006 Apr 30.
The Syrian hamster Harderian gland (HG) is a juxtaorbital organ exhibiting marked gender-associated morphological differences. Regarding contents of porphyrins, this gland is a good model for studying physiological oxidative stress effects, since both sexes present strong (in females) and moderate (in males) levels of this stress in normal conditions. We have recently showed that autophagic processes are in the Syrian hamster HG as the first result of an elevated porphyrin metabolism observed in both sexes. In this case, autophagy is not a cell death mechanism per se but a constant renovation system which allows to continuing with the normal gland activity. Moreover, we have also reported that this gland presents invasive processes, resembling to tumoral progression, and are, additionally, a consequence of a strong oxidative stress environment that is mainly observed in female Syrian hamster HG and in minor proportion in male HG. Here, we present additional data and discuss a model of melatonin action on these cited processes by which melatonin would be able to destroy the equilibrium between both detoxifying actions. We postulate that melatonin reduces oxidative stress level into HG as direct antioxidant. This decrease of free radicals produces the autophagy inhibition due to outbreak signal disappearance in HG. Under these events and regarding the huge contents of porphyrins that this gland supports, the invasive process triggers.
叙利亚仓鼠的哈德氏腺（HG）是一个眶旁器官，呈现出明显的性别相关形态差异。就卟啉含量而言，该腺体是研究生理氧化应激效应的良好模型，因为在正常情况下，两性均存在较强水平（雌性）和中等水平（雄性）的这种应激。我们最近发现，自噬过程在叙利亚仓鼠的哈德氏腺中存在，这是两性中观察到的卟啉代谢升高的首个结果。在这种情况下，自噬本身并非一种细胞死亡机制，而是一种持续更新系统，可使腺体维持正常活动。此外，我们还报告称，该腺体存在类似肿瘤进展的侵袭过程，并且这是主要在雌性叙利亚仓鼠哈德氏腺中观察到、在雄性哈德氏腺中占比小的强氧化应激环境的结果。在此，我们展示更多数据并讨论褪黑素对上述过程的作用模型，通过该模型褪黑素能够破坏两种解毒作用之间的平衡。我们推测，褪黑素作为直接抗氧化剂可降低哈德氏腺中的氧化应激水平。自由基的这种减少由于哈德氏腺中爆发信号消失而导致自噬抑制。在这些情况下，鉴于该腺体所支持的大量卟啉含量，侵袭过程被触发。
