Nucleotide bases
The five canonical nucleobases—adenine, cytosine, guanine, thymine, and uracil—that pair in DNA and RNA and anchor replication, repair, and epigenetic chemistry.
Key facts
The five canonical nucleobases—adenine, cytosine, guanine, thymine, and uracil—that pair in DNA and RNA and anchor replication, repair, and epigenetic chemistry.
- Which bases are in DNA versus RNA?
- DNA uses A, T, G, and C; RNA uses A, U, G, and C—uracil replaces thymine in RNA. Uracil in DNA is treated as damage and excised by repair enzymes.
Base chemistry clarifies mechanism pages under Vitamins (e.g. uracil misincorporation), links one-carbon metabolism to replication fidelity, and explains how oxidative and epigenetic lesions accumulate with age.
Adenine
Adenine is a purine base in DNA and RNA that pairs with thymine or uracil and anchors ATP, NAD+, and S-adenosylmethionine pools.
Purine balance affects nucleotide salvage versus de novo synthesis—relevant when oxidative stress or folate limitation shifts demand toward repair and remethylation. Chronic energy and cofactor stress can indirectly constrain adenylate pools that replication and epigenetic maintenance depend on.
Cytosine
Cytosine is a pyrimidine base that pairs with guanine; its methylation to 5-methylcytosine is central to epigenetic regulation and demethylation-linked mutation.
Cytosine chemistry links epigenetic aging clocks to mutation load—deamination and incomplete repair drive C→T transitions, a common somatic change with age. Folate and one-carbon status also intersect pyrimidine synthesis that replenishes cytosine in replicating genomes.
Guanine
Guanine is a purine base paired with cytosine; it is oxidation-sensitive and feeds GTP-dependent signaling and mitochondrial turnover.
Guanine oxidation is a direct readout of oxidative genomic instability. With age, cumulative 8-oxoG and imperfect base excision contribute to mutational burden in tissues with high metabolic flux.
Thymine
Thymine is the DNA pyrimidine (5-methyluracil) that replaces uracil in genomic DNA; its synthesis depends on folate-dependent thymidylate synthase.
Thymidylate pool size gates accurate DNA replication. When thymine synthesis lags, polymerases misinsert uracil, triggering excision–repair cycles that fragment chromosomes—a hallmark mechanism tied to folate deficiency.
Uracil
Uracil is an RNA pyrimidine base; when it appears in genomic DNA instead of thymine, repair enzymes treat it as damage.
Uracil itself is not a vitamin or supplement target—it is a nucleobase whose misplacement in DNA is a readout of cofactor status and replication stress. Understanding uracil clarifies why folate and B12 matter for thymidylate pools.