**5. Antioxidant treatment**

#### **5.1 Enzymatic therapies**

Animal studies have demonstrated the beneficial effects of SOD on ROS. SOD administration as aerosols in animals improved alveolar development in the case of bronchopulmonary dysplasia induced by the common action of multiple factors: prematurity, hyperoxia, and mechanical ventilation.

Cysteine, which has glutathione stimulating effects, was studied in premature babies. Glutathione is an important antioxidant and a cofactor for GPx. However, studies failed to demonstrate its beneficial effect in reducing oxidative stress, since the harmful effects of ROS could not be prevented by cysteine administration. Glutathione levels were significantly higher after cysteine administration. Administration of recombinant CuZnSOD to preterm babies during the intubation period led to a decrease in the incidence of wheezing episodes, but did not reduce the incidence of BPD compared to preterm babies who received placebo during the same period [20]. The incidence of ROP in preterm babies receiving this treatment also decreased [11].

#### **5.2 Non-enzymatic therapies**

The beneficial effects of vitamin E have been studied by different authors. Randomized controlled trials could not demonstrate the effect of vitamin E in preventing BPD. There are studies that evidence the beneficial effects of vitamin E in reducing the incidence of cerebral hemorrhage, while increasing the risk of neonatal sepsis; consequently, the risk exceeds the benefits provided by the antioxidant effect.

A Cochrane analysis of vitamin A describes its role in preventing BPD, but neurological and respiratory development at 18–22 months is not superior in babies receiving vitamin A [15, 21].

Regarding vitamin C, studies have demonstrated that in addition to its antioxidant effect, in certain situations, after a significant oxidative attack, vitamin C can act as a pro-oxidant and will cause additional injuries [13, 15].

High vitamin C concentrations will inhibit ceruloplasmin and will induce oxidation of Fe2+, which will have a catalytic action in lipid peroxidation and thus will generate new free radicals [23].

Excess of protein-unbound iron has a pro-oxidant effect, resulting in the production of free radicals with harmful effects. Lactoferrin has a key role in limiting the pro-oxidant action of free iron, its presence in milk formulas being particularly important [22, 28].

**193**

**Author details**

provided the original work is properly cited.

Melinda Matyas\* and Gabriela Zaharie

University of Medicine and Pharmacy, Cluj-Napoca, Romania

\*Address all correspondence to: melimatyas@yahoo.com

*Antioxidants at Newborns*

*DOI: http://dx.doi.org/10.5772/intechopen.85175*

activity counters the toxic effect of glutamate.

ity of breast milk is higher than that of neonatal blood [24].

Resveratrol is known for its antioxidant effect in astrocytes. Its role is important

Melatonin is a substance studied for its antioxidant effect. It has a role in repairing leukomalacia lesions, but its beneficial action has been described when it is administered early, in the first 2 hours after injury. Animal studies have demonstrated beneficial effects of enteral arginine and glutamine in preventing NEC [4, 5, 28]. Human milk feeding has a number of benefits over formulas. Studies demonstrate the antioxidant effect of breast milk, which contributes to ROS elimination. Higher amounts of oxidative stress metabolites are eliminated in the urine of preterm babies fed with formula compared to those fed with breast milk. Oxidative stress is increased in premature neonates fed with formula. The antioxidant capac-

after asphyxia episodes. It acts by stimulating glutamate synthase activity and increases GSH levels in hippocampal astrocytes. The increase in glutamate synthase

**5.3 Other antioxidant therapies**

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