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This combination transforms the molecule to its triplet form which by deactivation generates free radicals and a singlet oxygen from molecular oxygen, causing tumor destruction.
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It was found that molecular oxygen caused the decrease in the rate of N2O decomposition over all the catalysts studied under conditions of OCM.
Mainly at photosystem (PS) I but also at PSII, electron transfer reactions to molecular oxygen causes the production of superoxide anion radicals (O2.-), hydrogen peroxide (H2O2) and hydroxyl radicals (OH).
The combination of routine exposure of the cornea to UV-radiation and molecular oxygen may cause excessive production of reactive oxygen species (ROS), leading to substantial oxidative stress and subsequent tissue damage [1].
Molecular oxygen can causes alterations in the chemical structure of the bases in DNA.
Photodynamic therapy (PDT) uses photosensitive drugs (photosensitisers), combined with light and in the presence of molecular oxygen to cause tissue destruction.
Conversely, the downstream gene COX10 was upregulated and accompanied the overexpression of BcRISP1 to catalyze the transfer of electrons from reduced cytochrome c to molecular oxygen; this caused disruption of the mitochondrial electron transport chain because less electrons were produced due to the low expression of the upstream genes.
However, ROS is also generated as a by-product through the metabolism of molecular oxygen, and this causes damage to nucleotides, proteins, and lipids [ 16, 17].
The presence of oxygen causes deterioration of oxygen-sensitive foodstuffs.
A high oxygen content is undesirable, as oxygen causes undesirable oxidation reactions.
High-energy electrons produced in excess reduce molecular oxygen to generate ROS causing photosystem damage [ 9].
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