Brain Dev. 2007 Aug 31; [Epub ahead of print] Links
The evaluation of oxidative DNA damage in children with brain damage
using 8-hydroxydeoxyguanosine levels.
Fukuda M, Yamauchi H, Yamamoto H, Aminaka M, Murakami H, Kamiyama N,
Miyamoto Y, Koitabashi Y.
Department of Pediatrics, St. Marianna University School of Medicine,
2-16-1 Sugao, Miyamae-ku, Kawasaki 216-8511, Japan.
Urinary and cerebrospinal fluid (CSF) levels of 8-
hydroxydeoxyguanosine (8-OHdG) were examined to estimate the relevance
of oxidative stress in children with brain damage. Urinary 8-OHdG
levels were measured in 51 children with various forms of central
nervous system (CNS) disorders (status epilepticus [SE], hypoxic-
ischemic encephalopathy [HIE], CNS infections and chronic epilepsy)
and these levels were compared with those in 51 healthy children. CSF
8-OHdG levels were measured in 25 children with brain damage and in 19
control subjects. In addition, urinary and CSF levels of 8-OHdG were
compared between the children with brain damage and healthy children.
Finally, the relationship between urinary and CSF levels of 8-OHdG was
determined in 12 children that provided both urinary and CSF samples.
Our results showed that urinary 8-OHdG levels in children with HIE and
CNS infections were higher than those of controls (Steel test; p<0.05
and p<0.05, respectively) and that CSF 8-OHdG levels were higher in
children with SE, HIE, and CNS infections than in control subjects
(Steel test; p<0.01, 0.05 and 0.05, respectively). In addition, a
positive correlation between the levels of urinary and CSF 8-OHdG was
noted in the 12 children that provided both CSF and urinary samples
(Spearman's rank correlation; rho=0.82, p<0.01). Further, we observed
changes in the urinary 8-OHdG in a patient with HHV-6 encephalopathy,
and found that the changes correlated well with the patient's clinical
condition. These results suggest that oxidative stress is strongly
related to acute brain damage in children, and that 8-OHdG is a useful
marker of brain damage. Therefore, repeated measurements of urinary 8-
OHdG may be helpful in estimating the extent of brain damage.
PMID: 17766071 [PubMed - as supplied by publisher]
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Roman Bystrianyk - 05 Sep 2007 17:54 GMT
On Sep 5, 9:06 am, "ironjust...@aol.com" <ironjust...@aol.com> wrote:
> Brain Dev. 2007 Aug 31; [Epub ahead of print] Links
> The evaluation of oxidative DNA damage in children with brain damage
[quoted text clipped - 41 lines]
>
> DEAD PEOPLE WALKINGhttp://tinyurl.com/zk9fk
This is why a nutrient such as vitamin E can have a profound effect on
the brain.
Vitamin E (or -tocopherol / alpha-tocopherol) prevents the damaging
effects of oxidation in brain tissues. Free radical scavengers, such
as vitamin E, have been implicated in prolonged seizure activity.
Vitamin E is a natural nutrient that works to stabilize the membranes
of cells and has no known toxic effects. Early animal studies,
published in the Annals of Internal Medicine (3), found that rats and
mice that were exposed to 100% oxygen had seizures. However, the
authors found that they could prevent the seizures if they
administered vitamin E before the experiment. "Seizures occurred in
100% of the vitamin E deficient rats and in 50% of those fed a normal
diet, but none developed in rats fed a diet containing an -tocopherol
supplement."
In the journal Epilepsia (4), the authors of a study examined the
effect of vitamin E supplementation on 24 patients. The study was a
double-blind and placebo-controlled using 400 IUs of vitamin E for 3
months. At the end of the three months the authors found a dramatic
decrease in seizure activity in the patients taking the vitamin E
supplement.
"Of the 12 subject receiving active drug [vitamin E], 10 were
considered responders (> 60% reduction in seizure frequency), 6 had
90-100% reduction of seizure frequency, and 4 had 60-90% reduction.
Two were considered failures (< 60% reduction in seizure frequency).
The two failures were clinically identified as noncompliant subjects
during the trial period, and so confirmed by Vitamin E assays."
Not only was there a dramatic decrease in seizure activity, there was
even improvement in some of the patients' EEG measurements. "The EEG
findings, however, appeared to have improved in > 50% (four of seven
patients) of the responders who had EEG performed before and after
trial of add-on vitamin E."
After the 3 months, the 12 patients receiving the placebo were placed
on the vitamin E supplementation. Those 12 patients also showed
dramatic improvements by a "reduction in seizure frequency between 70
and 100% in all patients." Also, those patients that continued the
vitamin E protocol after the first 3 months continued to show
improvement. "[The] response of six subjects continuing vitamin E
after beneficial effects in the first phase [of the study] showed
continued improvement."
This study followed an older study published in Canadian Journal of
Neurological Sciences (5), where the author examined 100 children that
had grand mal seizures versus 100 healthy children. The author found
that those with the seizures had a much lower blood level of vitamin E
(632 g/dl [micrograms per deciliter) than those that did not have
seizures (822 g/dl). Here the author concluded that, "supplements of
-tocopherol might improve seizure control in such patients."
(3) High atmosphere pressures; physiological effects increased and
decreased pressure; application of these findings to clinical
medicine, A.R. Behnke, Annals of Internal Medicine, 1940, Vol. 13, pp.
2217-2228
(4) A Randomized, Double-Blind, Placebo-Controlled, Clinical Trial of
D-Alpha-Tocopherol Acetate (Vitamin E), as Add-On Therapy, for
Epilepsy in Children, A.O. Ogunmekan and P.A. Hwang, Epilepsia, 1989,
Vol. 30, No. 1, pp. 84-89
(5) Vitamin E Deficiency and Seizures in Animals and Man, A.O.
Ogunmekan, The Canadian Journal of Neurological Sciences, February
1979, Vol. 6, No. 1, pp. 43-45