Eukaryotic organisms constantly face a wide range of internal and external factors that cause damage to their DNA. Failure to accurately and efficiently repair these DNA lesions can result in genomic instability and the development of tumors (Canela et al., 2017). Among the various forms of DNA damage, DNA double-strand breaks (DSBs) are particularly harmful. Two major pathways, non-homologous end joining (NHEJ) and homologous recombination (HR), are primarily responsible for repairing DSBs (Katsuki et al., 2020; Li and Yuan, 2021; Zhang and Gong, 2021; Xiang et al., 2023). NHEJ is an error-prone repair mechanism that simply joins the broken ends together (Blunt et al., 1995; Hartley et al., 1995). In contrast, HR is a precise repair process. It involves multiple proteins in eukaryotic cells, with the RAD51 recombinase being the key player, which is analogous to bacterial recombinase A (RecA) (Shinohara et al., 1992). The central event in HR is the formation of RAD51-single-stranded DNA (ssDNA) nucleoprotein filaments that facilitate homology search and DNA strand invasion, ultimately leading to the initiation of repair synthesis (Miné et al., 2007; Hilario et al., 2009; Ma et al., 2017).
Recombinational DNA Repair ; DNA-Binding Proteins/metabolism* ; DNA Repair ; DNA Damage ; DNA

OBJECTIVETo explore the adduct characteristics of styrene and DNA.

METHODSThe adduct reactions between styrene, urinary mandalic acid(MA), phenylglyoxalic acid(PGA), mercapturic acid of styrene (UMA) and DNA were studied by ultraviolet spectral analysis. The SO-DNA adducts by 32P-post labeled method, the chemical structures of SO-DNA adducts by GC-MS and NMR were also studied.

RESULTSSO combined with DNA at O6, N2 positions of dGMP to form six adducts, but styrene, urinary mandalic acid, phenylglyoxalic acid and mercapturic acid of styrene did not react with DNA to form adduct.

CONCLUSIONSStyrene formed adduct with DNA through its active center metabolite--SO after entering the body. SO combined with DNA at O6, N2 positions of dGMP to form adducts. If these DNA adducts are not repaired or are mis-repaired before cell duplication, the gene mutation and chemical damage would happen. No adduct reactions are seen among other metabolites of styrene.

Acetylcysteine ; metabolism ; DNA ; metabolism ; DNA Adducts ; metabolism ; DNA Repair ; Glyoxylates ; metabolism ; Humans ; Mandelic Acids ; metabolism ; Styrene ; metabolism

The nature of hepatitis B virus (HBV) particle associated DNA polymerase was studied in relation to various enzyme inhibitors including antiviral agents. HBV DNA polymerase required high concentration of MgCl2(> 30 mM) and neutral pH for its full activity. p-chloromercuribenzoate was a strong inhibitor (85% inhibition at 1 mM) but N-ethylmaleimide had much less inhibitory effect (20% inhibition at 10 mM). Phosphonoformic acid showed the greatest inhibitory effect on HBV-DNA polymerase (almost complete inhibition at 100 microM) among phosphocompounds tested. Adenine arabinoside triphosphate (ara-ATP) and cytosine arabinoside triphosphate (ara-CTP) were competitive inhibitors with respect to their respective deoxyribonucleoside triphosphate (dATP and dCTP). Ara-CPT was a stronger inhibitor of HBV-DNA polymerase compared to ara-ATP. Ki values for ara-ATP and ara-CTP were 15.0 microM and 11.7 microM , respectively. HBV-DNA polymerase is characteristic in its ionic requirements and susceptibilities to certain inhibitors.
DNA-Directed DNA Polymerase/antagonists & inhibitors ; DNA-Directed DNA Polymerase/metabolism* ; Hepatitis B Virus/enzymology* ; Human

Animals ; Mice ; DNA Repair ; DNA Breaks, Double-Stranded ; DNA/metabolism* ; DNA Damage

TAR DNA-binding domain protein 43 （TDP-43） is a highly conserved and widely expressed nuclear protein. Nowadays, the expression of TDP-43 can be found in most neurodegenerative diseases such as Alzheimer's disease, which makes it become a neurodegenerative disease associated marker protein. From the current research status at homeland and abroad, and around the relationship between the expression of TDP-43 and brain injury, this article emphatically probes into the specific expression and function of TDP-43 in acute and chronic brain injury based on the knowledge of its biological characteristics, which aims to explore the feasibility for determining the cause of death and the injury and disability situations by TDP-43 in forensic pathology.
Brain Injuries/pathology* ; DNA ; DNA-Binding Proteins/metabolism* ; Humans

DNA Damage ; DNA Glycosylases ; genetics ; metabolism ; DNA Repair Enzymes ; genetics ; metabolism ; Humans ; Phosphoric Monoester Hydrolases ; genetics ; metabolism

Eukaryotic cells contain numerous iron-requiring proteins such as iron-sulfur (Fe-S) cluster proteins, hemoproteins and ribonucleotide reductases (RNRs). These proteins utilize iron as a cofactor and perform key roles in DNA replication, DNA repair, metabolic catalysis, iron regulation and cell cycle progression. Disruption of iron homeostasis always impairs the functions of these iron-requiring proteins and is genetically associated with diseases characterized by DNA repair defects in mammals. Organisms have evolved multi-layered mechanisms to regulate iron balance to ensure genome stability and cell development. This review briefly provides current perspectives on iron homeostasis in yeast and mammals, and mainly summarizes the most recent understandings on iron-requiring protein functions involved in DNA stability maintenance and cell cycle control.
Animals ; Cell Cycle Checkpoints ; DNA ; metabolism ; DNA Repair ; DNA Replication ; Hemeproteins ; genetics ; metabolism ; Iron ; chemistry ; metabolism ; Iron-Sulfur Proteins ; genetics ; metabolism ; Ribonucleotide Reductases ; genetics ; metabolism ; Yeasts ; metabolism

We investigated toluene exposure level, urinary hippuric acid concentrations, subjective symptoms and genotype of ALDH2 DNA in 134 exposed workers and 53 nonexposed workers for evaluating the effect of ALDH2 polymorphism on toluene metabolism and urinary hippuric acid concentration as biological exposure indices (BEI) of toluene. The results were as follows; 1. The percentage of inactive genotype of ALDH2 in exposed workers was lower than that of exposed (P=0.081). 2. The percentages of exposed workers with inactive genotype did not have any significant difference by the increase of toluene exposure level or work duration. 3. The frequency of drinking, monthly and maximum amount of alcohol intake in workers with normal genotype were significantly higher than those with inactive genotype. 4. The urinary hippuric acid concentration of nonexposed workers ,with inactive genotype was significantly lower than that with normal genotype. Under 100 ppm of toluene, similar but statistically insignificant trends were found, while above that concentration of toluene, reverse but statistically insignificant trends were found. 5. The number of acute and chronic subjective symptoms were increased positively with the concentration of toluene in workers with normal genotype, but ho such trends were found in workers with inactive genotype. 6. The result of simple linear regression between toluene and urinary hippuric acid concentrations showed a very significant positive linear relation-ship. The mean hippuric acid concentration of nonoccupational exposure was 0.289+/-0.227 (0.062-0.516) g/l. Toluene exposure level unable to discriminate with nonoccupational exposure estimated from regression equation, it range from 7.29 to 9.87 ppm. Considering above all things, it was useful to estimate the exposure level of toluene by means of analysing urinary hippuric acid concentration in both genotype workers, but the biological exposure indices (BEI) of both genotypes were different from each other. The BEI of the total exposed workers was 2.76 g/ I, which was lower than current criteria 3.0g/ I (2.5 g/g Cr), and it also suggest that the BEI for the exposed workers in our country be lowered to the appropriate level after further study.
DNA ; Drinking ; Genotype* ; Linear Models ; Metabolism ; Toluene*

8-oxo-7,8-dihydroguanine (8-oxo-G) in DNA is a mutagenic adduct formed by reactive oxygen species. In Escherichia coli, 2,6-dihydroxy-5N-formamidopyrimidine (Fapy)-DNA glycosylase (Fpg) removes this mutagenic adduct from DNA. In this report, we demonstrate base excision repair (BER) synthesis of DNA containing 8-oxo-G with Fpg in vitro. Fpg cut the oligonucleotide at the site of 8-oxo-G, producing one nucleotide gap with 3' and 5' phosphate termini. Next, 3' phosphatase(s) in the supernatant obtained by precipitating a crude extract of E. coli with 40% ammonium sulfate, removed the 3' phosphate group at the gap, thus exposing the 3' hydroxyl group to prime DNA synthesis. DNA polymerase and DNA ligase then completed the repair. These results indicate the biological significance of the glycosylase and apurinic/ apyrimidinic (AP) lyase activities of Fpg, in concert with 3' phosphatase(s) to create an appropriately gapped substrate for efficient BER synthesis of DNA containing 8-oxo-G.
DNA Glycosylases/metabolism ; *DNA Repair ; DNA, Bacterial/*chemistry/*metabolism ; DNA-Formamidopyrimidine Glycosylase/metabolism ; Escherichia coli/*enzymology/*genetics ; Guanine/*analogs & derivatives/*metabolism

DNA/metabolism* ; Gene Editing ; HEK293 Cells ; Humans