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1 ts antimicrobial activity is due to damaging cellular macromolecules.
2 nd these reactive oxygen species can oxidize cellular macromolecules.
3 rcalate into membranes and promote damage to cellular macromolecules.
4 st synthesize all of the building blocks for cellular macromolecules.
5 d to be sufficient to suppress catabolism of cellular macromolecules.
6 d the vibrational contributions of the other cellular macromolecules.
7 cation of reactive aldehydes that can modify cellular macromolecules.
8 y react with vital parasite thiol-containing cellular macromolecules.
9 aerobes is the stage for biosynthesis of all cellular macromolecules.
10 s that challenge homeostasis by crosslinking cellular macromolecules.
11 without altering the functional activity of cellular macromolecules, a property defining it as a "co
15 mary mode of cancer therapy, acutely damages cellular macromolecules and DNA and elicits stress respo
16 quine quinoneimine (AQQI), which can bind to cellular macromolecules and initiate hypersensitivity re
17 catabolic cellular mechanism for entrapping cellular macromolecules and organelles in intracellular
18 ainst covalent modification of DNA and other cellular macromolecules by BPDE was modeled in human T47
19 ive cell injury involves the modification of cellular macromolecules by reactive oxygen intermediates
20 Altered structure, and hence function, of cellular macromolecules caused by oxidation can contribu
21 to generate three-dimensional structures of cellular macromolecule complexes in their native environ
22 acellular localization of proteins, studying cellular macromolecule delivery vehicles, studying cell-
23 ugh reactive oxygen species (ROS) may damage cellular macromolecules directly, oxidant-induced cell d
24 roteins play an important role in protecting cellular macromolecules from damage by reactive oxygen s
26 otypes through their interactions with other cellular macromolecules including DNA, protein, and RNA.
27 normal mitochondrial respiration can damage cellular macromolecules, including mitochondrial DNA (mt
28 We hypothesize that many modifications in cellular macromolecules, observed in cancer progression,
29 tive oxygen molecules that can interact with cellular macromolecules (proteins, lipids, nucleic acids
30 oduction of the two most abundant classes of cellular macromolecules, proteins, and nucleic acids in
31 itroimidazole EF5, which covalently binds to cellular macromolecules selectively under hypoxic condit
32 tion, can have a profound negative effect on cellular macromolecules such as DNA that may lead to a n
33 e the biases in the spatial distributions of cellular macromolecules that result from the integrated
35 ing nutrient stress, macroautophagy degrades cellular macromolecules, thereby providing biosynthetic
36 Autophagy is a catabolic process that allows cellular macromolecules to be broken down and re-utilize
37 Autophagy is a catabolic process that allows cellular macromolecules to be broken down and recycled a
38 desiccation tolerance mechanisms to protect cellular macromolecules under anhydrobiosis, with second