Abstract
Growth Arrest and DNA Damage-inducible 45 (Gadd45) and MDM2 proteins, together with p21 and p53, play important roles in cell cycle checkpoints, DNA repair, and genome integrity maintenance. Gadd45 and MDM2 were activated and transcribed instantly by UV irradiation, whereas blueberry anthocyanins (BA) decreased the gene and protein expression levels in HepG2 cells for up to 24 h, and gradually restored the UV-induced fragmented and non-fragmented DNA damage of the nucleus at a time point of 12 h. Nevertheless, UV-irradiated HepG2 cell arrests occurred mainly in the G1 phase, which indicated G1 as a checkpoint. The proteins, p21 and p53, retain cellular integrity, suppressing the oncogenic transformation by interruption of the G1 phase of the cellular cycle, giving time for repairing the damage to DNA, or apoptosis induction if the damage is too severe to be repaired, while MDM2 and Gadd45 concomitantly ensure the presence of p53 and p21. Thus, we conclude that repair, together with Gadd45 and MDM2 genes, were involved in light and dark reaction mechanisms, however, BA could interfere and assist the repair through restoration, although further studies of the complex of the gene cascades triggered and responded to in BA-assisted DNA repair are needed.
Highlights
When cellular and tissue environments are favorable, cells initiate their division cycle by DNA synthesis and tighten surveillance
The scanning electron microscope (SEM) results demonstrated that the UV-irradiated group appeared wrinkled, curled, and with blisters, whereas blueberry anthocyanins (BA) treatment alleviated UV-extended damage compared with the control cell group, which had cellular integrity and clear surface morphology (Figure 2)
The DNA fragmented damage by fluorescence of the tail moment was digitally analyzed using CASP software (Figure 6f). These results indicated that pre-treatment with BA significantly decreased the level of DNA damage compared with the control group in a concentration-dependent manner
Summary
When cellular and tissue environments are favorable, cells initiate their division cycle by DNA synthesis and tighten surveillance. Several cell cycle checkpoints are imposed to monitor the accuracy of the cell cycle events, with the option to halt the cell cycle at virtually any transition point if a major malfunction or DNA damage is encountered [1]. Failure to execute these cell cycles accurately signifies that the cell cycle checkpoints may lead to devastating consequences, such as cancer. Checkpoint controls arrest the cell cycle after DNA damage, frequently allowing repair to take place before mutations can be perpetuated [2,3,4,5]. Among the cell cycle of three checkpoints, G1 regulation has attracted significant attention in radiobiology
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