Cell death is on the origin of degenerative diseases such as Parkinson. Taking this as starting point, Darío Acuña Castroviejo´s group, of the Department of Physiology of the UGR, studies the mechanisms which take part in this process, connecting cell death with damages in the mitochondria, its power source. In tests on animals and cell cultures, scientists have confirmed that melatonin, a hormone produced in all the organs of the human body, can protect cells from the attacks that cause its death, as well as prevent mitochondrial malfunction.
After several years of work, this team of scientists has observed that cell death is connected to the increase of nitric oxide and free radicals in the cell mitochondria. Our organism produces these substances naturally, but when they reach excessive levels they become toxic. When a cell dies, it releases nitric oxide and free radicals which can also attack other brain cells. Thus, an inflammatory chain reaction can be unleashed; in the case of Parkinson, it would be the cause of the black substance. This part of the brain modulates movement through a series of connections, regulated by means of a neurotransmitter substance, dopamin. Therefore, when Parkinson affects it motor problems appear.
UGR researchers think that the inflammatory process is on the basis of the mithocondrial damage suffered cells of the black substance. Thus, “if mithocondrial was avoided cell death could be avoided too”, sums up the researcher. Melatonin could be the solution, a hormone naturally produced by our organism with well-known neuroprotective properties. The scientists of the University of Granada have discovered that the mitochondria can keep 300 times more melatonin than that found in blood. “Melatonin can inhibit nitric oxide production in the mitochondria in these inflammatory neurodegenerative processes”, reveals Darío Acuña.
Mitochondria protection
Scientists have used this hormone as a medicine in two models. One of them recreates Parkinson. The researchers have confirmed that melatonin decreases nitric oxide and protects the mitochondria. Now they intend to measure the most complex parameters, like energy production. Acuña thinks that it will allow to observe better the capacity of melatonin to counteract the damages in the mitochondria. In collaboration with another UGR researcher, Antonio Espinosa, Acuña´s team has studied a series of molecules synthesized from the structure of natural melatonin, observing that, in laboratory cell cultures, they can inhibit the enzyme which increases nitric oxide in the mitochondria.
“The therapeutic expectations of melatonin are enormous”, points out Acuña. And he adds: “In view of the benefits and the fact that other countries take advantage of the basic research work carried out in Spain, it is an absurdity to forbid the therapeutic use of melatonin in patients, always in the framework of a medical control”.
Reference: Prof. Darío Acuña Castroviejo. Dpt. Physiology. Institute of Biotechnology.
Phone numbers: 958 246 631.
Mobile: 616 929 320.
E-mail: dacuna@ugr.es.
