Head trauma causes two kinds of injury in the neural tissue. One is the pri
mary injury which occurs at the time of impact. The other one is a secondar
y injury and is a progressive process. Free radicals are produced during ox
idative reactions formed after trauma. They have been thought to be respons
ible in the mechanism of the secondary injury. Some studies have been condu
cted to demonstrate the role of free oxygen radicals in neuronal injury. Th
e alterations in the free radical level during the early posttraumatic peri
od and the effect of a free radical scavenger on these alterations have not
been studied as a whole. We aimed to demonstrate the free oxygen radical l
evel changes in the early posttraumatic period and the effect of melatonin,
which is a potent free radical scavenger, on the early posttraumatic free
radical level. A two-staged experimental head trauma study was designed. In
stage one, post-traumatic free radical level changes were determined. In t
he second stage, the effect of melatonin on the free radical level changes
in the post-traumatic period was studied. Two main groups of rats each divi
ded into four subgroups were studied. Rats in one of the main groups underw
ent severe head trauma, and malondealdehyde (MDA) levels were measured in t
he contused cerebral tissue at different time points. Rats in the other mai
n group also underwent the same type of trauma, and melatonin was injected
intraperitoneally at different time points after trauma. The MDA level alte
ration in the tissue was determined after the injection of melatonin. The M
DA level increased rapidly in the early posttraumatic period. But in time,
it decreased in the groups with only trauma. In the melatonin-treated group
, the MDA level decreased after the injection of melatonin, when injected i
n the early posttraumatic period, compared to the control and trauma groups
. However, melatonin increased MDA to a higher level than in the groups wit
h only trauma and the control group when injected later than 2 h after trau
ma. The MDA level increases in the very early posttraumatic period of cereb
ral trauma and decreases in time. Melatonin, which is the most potent endog
enous free radical scavenger, when injected intraperitoneally to the cerebr
al traumatized rats in the very early posttraumatic period, causes a signif
icant decrease in the MDA level. But, melatonin, when injected more than 2
h after trauma, increases the MDA level in experimental cerebral trauma in
rats. Copyright (C) 2000 S. Karger AG, Basel.