DNA breaks and oxidative guanosine are higher in arterial hypertension compared to controls

Introduction Three types of oxidative DNA damage ((oxidised guanosine/8OHdG, Single strand breaks (SSBs)/comet assay, Double strand breaks (DSBs)/gammaH2AX)) are becoming tested more frequently in clinical cardiology research (Picture 1). Epidemiology of arterial hypertension /HT/ is not optimal. Purpose To describe systematically the most severe DNA damage in HT (humans, animals, cell-lines). Methods This review on DNA damage in HT was made using multiple databases to search for English-language publications up to June 30, 2022 and the key words: DNA damage, 8OHdG, strand breaks, comet assay, gammaH2AX and HT. Inclusion, exclusion criteria, flow diagram (Picture 1). Results Finally, N=31 studies: (N=15 humans, N=13 animals, N=3 cells) (Picture 1). A total of 902 hypertensive patients (pts): (8OHdG: N=484 pts; SSBs: N=418 pts) and 587 controls (8OHdG: N=384; SSBs: N=203) were included. DNA damage was significantly higher in hypertensive pts than healthy controls (8OHdG 13.1±4.12 vs 6.97±2.67 ng.mg-1 creatinine; P<0.05 and SSBs 26.6±11.0 vs 11.7±4.07 arbitrary units /A.U./; P<0.05) with the average mean differences and 95% confidence limit (MD /95%CL) 7.5 /6.6; 8.6/ ng.mg-1 creatinine for 8OHdG in urine, respectively 14.7 /6.4; 23.0/ A.U. for SSBs in peripheral lymphocytes. Greater DNA damage was observed in more adverse cases (sustained/untreated hypertension 31.4±12.1 vs 14.2±5/35.0±5.0 vs 25.0±5.0; non-dippers 39.2±15.5 vs 29.4±11.1 A.U.; concentric cardiac hypertrophy 43.4±15.4 vs 15.6±5.5; elderly 14.9±4.5 vs 9.3±4.1 ng.mg-1 creatinine; without carvedilol 9.1±4.2 vs 5.7±3.9; with coronary heart disease 0.5±0.1 vs 0.2±0.1 ng.mL-1) (P<0.05) with the average MD /95% CL/ 3.4 /0.8;5.9/ ng.mg-1 creatinine for 8OHdG in urine, respectively 16.1 /12.1; 20.1/ A.U. for SSBs in peripheral lymphocytes. DNA damage correlated strongly positively with serum glycosylated haemoglobin (r=0.670; P<0.05) and negatively with total antioxidant status (r=−0.670 to −0.933; P<0.05). Higher DNA damage (8OHdG, SSBs, DSBs; P<0.05) in HT than in controls was consistently seen also under strictly experimental conditions (animals; cell-lines). Conclusion This is the first review showing systematically that oxidative DNA damage was consistently increased in HT individuals compared to controls (humans, animals, cell-lines) (Ref 1;2). The author believes that this finding can help at least partially fill in the gaps in the evidence, it can be a further piece in the pathophysiological subcellular mosaic (unrepaired harmful DNA in the cytosol when the reparation and defences are exceeded, cytosolic DNA sensors are activated) (Ref 3;5). Thus author believes, that this finding could represent a new therapeutic challenge (DNA damage response substances like a target) (Ref 4;5). First of all, everything must be thoroughly and repeatedly investigated with the caution for pharmacotherapy (Ref 1;2), which can unfortunately affect the results of DNA damage (Ref 1;6).