Could melatonin unbalance the equilibrium between autophagy and invasive processes?

The Syrian hamster Harderian gland (HG) is a juxtaorbital organ exhibiting marked gender-associated morphological differences. Due to alterations in the contents of porphyrins, this gland is a good model for studying physiological oxidative stress effects, since both sexes display strong (in females) and moderate (in males) levels of this stress in normal conditions. We recently showed that autophagic processes occur in the Syrian hamster HG as the first result of an elevated porphyrin metabolism observed in both sexes. In this case, autophagy functions in a protective role, serving as a constant renovation system, which allows continuation of normal gland activity. Moreover, we have also reported that this gland develops invasive processes, through a mechanism that resembles tumor progression. As with autophogy, these invasive structures serve a protective role and are a consequence of a strong oxidative stress environment that is mainly observed in female Syrian hamster HG and only in minor proportion in male HG. Here, we present additional data and discuss a model of melatonin action on these processes by which melatonin would be able to destroy the equilibrium between both detoxifying actions. We postulate that melatonin reduces the oxidative stress level in HG, acting as a direct antioxidant. The subsequent decrease of free radicals inhibits autophogy by removing the inducing signal from the HG. Under these circumstances, the invasive process is triggered due to the huge content of porphyrins that this gland maintains.