以微量體液化學發光法定量早產兒血液中活性氧及抗氧化狀態來評估與視網膜病變嚴重度之相關性(2/2)
Date Issued
2005
Date
2005
Author(s)
謝武勳
DOI
932314B002047
Abstract
Neonates undergo a dramatic change during the process of childbirth by an increase in
oxidative aggression. The fetus exchange a low oxygen intrauterine environment, with PO2 of
20-25 mmHg and a low presence of free radicals, for another with a relative high oxygen
extrauterine environment, with PO2 of 100 mmHg. This change results in considerable oxidative
stress.
Damage due to free radicals, including reactive oxygen species and reactive nitrogen
species, is thought to be one of the common mechanisms for several neonatal diseases especially
in preterm infants. Chronic lung disease of neonate, retinopathy of prematurity, necrotizing
enterocolitis, and hemolytic diseases of neonate are accepted as caused by the excessive
production of oxygen or nitrogen free radicals. The oxidative aggression suffered by the neonate
is counteracted by the maturation of complex antioxidant defense systems, including both
enzymatic systems (superoxide dismutase, catalase, glutathione peroxidase, etc.), and
non-enzymatic systems (vitamins E, A, C ). Despite the knowledge that has been advanced in
recent years regarding the oxidative stress and antioxidant mechanism, there have remained
questions about the maternal-fetal transfer of antioxidant defense mechanism and the free
radical and antioxidant status in neonates during perinatal period.
Retinopathy of prematurity (ROP) is a disease of the incompletely vascularized immature
reteina characterized by retinovitreal neovascularization. It develops in more than 80% of
premature survivors born at <28 weeks gestation. Some evidences, by estimating the
associations between protein oxidation and lipid peroxidation products and retinopathy of
prematurity, indirectly suggest that reactive oxygen species and reactive nitrogen species may
play important roles in the pathogenesis of ROP. However, direct evidence that oxidation plays a
causative role in ROP is limited. It is not always clear whether the association between oxygen
and ROP just reflect a higher disease incidence in the very-low- birth-weight infants who
receive more oxygen. Besides, the assay procedures of protein oxidation and lipid peroxidation
products may be different and nonspecific, newer and more sensitive tests is warranted.
We have developed to use a characteristic emission spectrum analysis of the
chemiluminescence (CL-spectrum) with small amount of body fluids for the first time to
evaluate the specific reactive oxygen species (ROS) activity including H2O2 and HOCl in the
plasma and to adapt a chemiluminescence-high performance liquid chromatography (CL-HPLC)
for measurement of PCOOH before and after the dialysis session, in the absence and presence of
antioxidant treatment.
We hypothesize that the contents of free radicals and the antioxidant defense system are
III
different between the preterm infants with ROP and those without ROP. We propose a two-year
research project.
During the first year of our study, 10 preterm and 14 term infants had been enrolled. We
found that the plasma ROS level was significantly higher then those of the cord blood. However,
the levels were not affected by the gestational age, the gender and the mode of delivery. The
elevation was supposed due to the oxidative stress after the birth.
During the second year of our study, we continually collected the tears from the preterm
infants. Totally 45 infants were enrolled including 41 infants without retinopathy of prematurity
and 4 infants with retinopathy of prematurity. We found that the plasma ROS levels at the age of
three says were also significantly elevated after birth when compared with those of the cord
blood both in the preterm infants with ROP and those without ROP. This result was compatible
with our first year study. Again, we believed that the neonates suffered from oxidative stress
after birth.
In the analysis of ROS in tears of the preterm infants, we found that both of the
Luminol-dependent ROS and Lucigen-dependent ROS were not significantly different at the 7,
14, 21, 28, 35, 42 and 49 days of age. The difference was significant at the eighth week of age.
We speculated that the difference was associated with the development of ROP. However, that
collection of the tears from the preterm infants was not satisfactory and the amount of the tears
was usually limited. The limitation of the samples collection may substantially affect the results
of our study. Further improved methods for the analysis of tears ROS is necessary for the
interpretation of the pathophysiology of ROP.
oxidative aggression. The fetus exchange a low oxygen intrauterine environment, with PO2 of
20-25 mmHg and a low presence of free radicals, for another with a relative high oxygen
extrauterine environment, with PO2 of 100 mmHg. This change results in considerable oxidative
stress.
Damage due to free radicals, including reactive oxygen species and reactive nitrogen
species, is thought to be one of the common mechanisms for several neonatal diseases especially
in preterm infants. Chronic lung disease of neonate, retinopathy of prematurity, necrotizing
enterocolitis, and hemolytic diseases of neonate are accepted as caused by the excessive
production of oxygen or nitrogen free radicals. The oxidative aggression suffered by the neonate
is counteracted by the maturation of complex antioxidant defense systems, including both
enzymatic systems (superoxide dismutase, catalase, glutathione peroxidase, etc.), and
non-enzymatic systems (vitamins E, A, C ). Despite the knowledge that has been advanced in
recent years regarding the oxidative stress and antioxidant mechanism, there have remained
questions about the maternal-fetal transfer of antioxidant defense mechanism and the free
radical and antioxidant status in neonates during perinatal period.
Retinopathy of prematurity (ROP) is a disease of the incompletely vascularized immature
reteina characterized by retinovitreal neovascularization. It develops in more than 80% of
premature survivors born at <28 weeks gestation. Some evidences, by estimating the
associations between protein oxidation and lipid peroxidation products and retinopathy of
prematurity, indirectly suggest that reactive oxygen species and reactive nitrogen species may
play important roles in the pathogenesis of ROP. However, direct evidence that oxidation plays a
causative role in ROP is limited. It is not always clear whether the association between oxygen
and ROP just reflect a higher disease incidence in the very-low- birth-weight infants who
receive more oxygen. Besides, the assay procedures of protein oxidation and lipid peroxidation
products may be different and nonspecific, newer and more sensitive tests is warranted.
We have developed to use a characteristic emission spectrum analysis of the
chemiluminescence (CL-spectrum) with small amount of body fluids for the first time to
evaluate the specific reactive oxygen species (ROS) activity including H2O2 and HOCl in the
plasma and to adapt a chemiluminescence-high performance liquid chromatography (CL-HPLC)
for measurement of PCOOH before and after the dialysis session, in the absence and presence of
antioxidant treatment.
We hypothesize that the contents of free radicals and the antioxidant defense system are
III
different between the preterm infants with ROP and those without ROP. We propose a two-year
research project.
During the first year of our study, 10 preterm and 14 term infants had been enrolled. We
found that the plasma ROS level was significantly higher then those of the cord blood. However,
the levels were not affected by the gestational age, the gender and the mode of delivery. The
elevation was supposed due to the oxidative stress after the birth.
During the second year of our study, we continually collected the tears from the preterm
infants. Totally 45 infants were enrolled including 41 infants without retinopathy of prematurity
and 4 infants with retinopathy of prematurity. We found that the plasma ROS levels at the age of
three says were also significantly elevated after birth when compared with those of the cord
blood both in the preterm infants with ROP and those without ROP. This result was compatible
with our first year study. Again, we believed that the neonates suffered from oxidative stress
after birth.
In the analysis of ROS in tears of the preterm infants, we found that both of the
Luminol-dependent ROS and Lucigen-dependent ROS were not significantly different at the 7,
14, 21, 28, 35, 42 and 49 days of age. The difference was significant at the eighth week of age.
We speculated that the difference was associated with the development of ROP. However, that
collection of the tears from the preterm infants was not satisfactory and the amount of the tears
was usually limited. The limitation of the samples collection may substantially affect the results
of our study. Further improved methods for the analysis of tears ROS is necessary for the
interpretation of the pathophysiology of ROP.
Subjects
prematurity
neonate
respiratory distress syndrome
patent ductus arteriosus
chronic lung disease reactive oxygen species
reactive nitrogen species
free radical
antioxidant status
retinopathy of prematurity
chemiluminescence
Publisher
臺北市:國立臺灣大學醫學院小兒科
Type
report
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