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Excess hydrogen peroxide inhibits head and foot regeneration in hydra by affecting DNA repair and expression of essential genes
Author(s) -
Haval Gauri A.,
Pekhale Komal D.,
Perween Nusrat A.,
Ghaskadbi Surendra M.,
Ghaskadbi Saroj S.
Publication year - 2020
Publication title -
journal of biochemical and molecular toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.526
H-Index - 58
eISSN - 1099-0461
pISSN - 1095-6670
DOI - 10.1002/jbt.22577
Subject(s) - lernaean hydra , regeneration (biology) , reactive oxygen species , wnt signaling pathway , base excision repair , microbiology and biotechnology , dna damage , hydrogen peroxide , dna repair , chemistry , gene , biology , signal transduction , biochemistry , dna
Reactive oxygen species (ROS) are necessary for various cellular processes. However, excess ROS cause damage to many biological molecules and therefore must be tightly regulated in time and space. Hydrogen peroxide (H 2 O 2 ) is the most commonly used ROS as second messenger in the cell. It is a relatively long‐lived freely diffusible signaling molecule during early events of injury. In the Cnidarian hydra, injury‐induced ROS production is essential for regeneration to proceed. In the present study, we have examined influence of varying exposure to H 2 O 2 on head and foot regeneration in the middlepieces of trisected hydra. We find that longer (4 hours) exposure to 1 mM H 2 O 2 inhibits both head and foot regeneration while shorter exposure (2 hours) does not. Longer exposure to H 2 O 2 resulted in extensive damage to DNA that could not be repaired, probably due to suboptimal induction of APE1, an enzyme necessary for base excision repair (BER). Concomitantly, genes involved in activation of Wnt pathway, necessary for head regeneration, were significantly downregulated. This appeared to be due to failure of both stabilization and transient nuclear localization of β‐catenin. Similarly, genes involved in foot regeneration were also downregulated on longer exposure to H 2 O 2 . Thus, exposure to excess ROS inhibits regenerative processes in hydra through reduced expression of genes involved in regeneration and diminished DNA repair.