Melatonin expression in periodontal disease

It was the purpose of this study to examine the relationship between periodontal diseases and melatonin level. Material and Methods:  Forty-six patients with periodontal disease, together with 26 age- and gender-matched healthy controls, were included. Periodontal status was assessed using the Community Periodontal Index. Plasma and salivary melatonin levels were determined using specific commercial radioimmunoassays, whereas lymphocyte subpopulations (e.g. CD3, CD4, CD8, C19 and natural killer cells) were analyzed using flow cytometry. Results:  Patients with periodontal disease had significantly ( p <  0.001) lower plasma (9.46 ± 3.18 pg/mL) and saliva (2.55 ± 0.99 pg/mL) melatonin levels than healthy control patients (14.33 ± 4.05 and 4.22 ± 0.87 pg/mL, respectively). A biphasic relationhip was observed between plasma melatonin levels and Community Periodontal Indices. The plasma melatonin level was reduced in patients with a lower Community Periodontal Index value (1 or 2) and increased in patients with a higher Community Periodontal Index value (3 or 4). Salivary melatonin parallels the changes of plasma melatonin. The higher the Community Periodontal Index, the older the patient and the higher the total lymphocyte counts. CD4 concentrations also increased as the disease worsened. Conclusion:  The results obtained from this study suggest that melatonin could act as a protective function in fighting periodontal infection. However, further studies in this area are encouraged.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/65967/1/j.1600-0765.2007.00978.x.pd

A922 Sequential measurement of 1 hour creatinine clearance (1-CRCL) in critically ill patients at risk of acute kidney injury (AKI)

Meeting abstrac

MELATONIN ANTAGONIZES THE INTRINSIC PATHWAY OF APOPTOSISVIA MITOCHONDRIAL TARGETING OF Bcl-2

We have recently shown that melatonin antagonizes damage-induced apoptosis by interaction with the MT-1/MT-2 plasma membrane receptors. Here, we show that melatonin interferes with the intrinsic pathway of apoptosis at the mitochondrial level. In response to an apoptogenic stimulus, melatonin allows mitochondrial translocation of the pro-apoptotic protein Bax, but it impairs its activation/dimerization The downstream apoptotic events, i.e. cytochrome c release, caspase 9 and 3 activation and nuclear vesiculation are equally impaired, indicating that melatonin interferes with Bax activation within mitochondria. Interestingly, we found that melatonin induces a strong re-localization of Bcl-2, the main Bax antagonist to mitochondria, suggesting that Bax activation may in fact be antagonized by Bcl-2 at the mitochondrial level. Indeed, we inhibit the melatonin anti-apoptotic effect (i) by silencing Bcl-2 with small interfering RNAs, or with small-molecular inhibitors targeted at the BH3 binding pocket in Bcl-2 (i.e. the one interacting with Bax); and (ii) by inhibiting melatonin-induced Bcl-2 mitochondrial re-localization with the MT1/MT2 receptor antagonist luzindole. This evidence provides a mechanism that may explain how melatonin through interaction with the MT1/MT2 receptors, elicits a pathway that interferes with the Bcl-2 family, thus modulating the cell life/death balance

Melatonin: new places in therapy

The fact that the full extent of the function of the pineal gland has not yet been elucidated, has stimulated melatonin research worldwide. This review introduces melatonin's mechanism of action, direct and indirect antioxidant actions as well as the antioxidant properties of its metabolites, 6-hydroxymelatonin (6-OHM) and N-acetyl-N-formyl-5-methoxykynurenamine (AFMK). At present the mechanism of action is proposed to be receptor-, protein- and nonprotein-mediated. From its popular role in the treatment of jetlag, melatonin is now implicated in the reduction of oxidative stess, both as a free radical scavenger and antioxidant. Melatonin's direct scavenging action in respect of the following will be discussed: superoxide anions, hydrogen peroxide, hydroxyl radicals, singlet oxygen, peroxy radicals and nitric oxide/peroxy nitrite anions. In addition melatonin also possesses indirect antioxidant activity and the role of its metabolites, AFMK and 6-OHM will be presented. It is these free radical scavenging and antioxidant properties of melatonin that has shifted the focus from that of merely strengthening circadian rhythms to that of neuroprotectant: a new place in therapy