Phytochemistry and Antigenotoxic Properties of Six Ethnobotanically Important Members From the Family Zingiberaceae

2022 ◽  
pp. 378-400
Author(s):  
Anish Nag
Keyword(s):  
Antioxidant Properties ◽  
Zingiber Officinale ◽  
Dna Strand Breaks ◽  
Herbal Extracts ◽  
Strand Breaks ◽  
Phytochemical Composition ◽  
Curcuma Amada ◽  
Dna Damaging Agents ◽  
The Family ◽  
Dna Strand

Genotoxicity is considered as a potential cause of various diseases including cancer. During the last decade, herbal extracts attained a great deal of attention due to its safe and effective applications against various DNA damaging agents. However, the mechanism of DNA strand breaks by various mutagens and genotoxins is often correlated with the generation of Reactive Oxygen Species (ROS). Herbal extracts constitute a number of phytochemicals and those are reported to have considerable antioxidant properties, which are in turn capable of neutralizing ROS mediated DNA damage. The botanical family Zingiberaceae is reported to have significant antioxidant and antigenotoxic potential by various researchers. Among a number of species belonging to this family, six species, namely Alpinia galanga, A. zerumbet, Curcuma amada, C. caesia, Zingiber officinale, and Z. zerumbet, attract notable attention due to their remarkable ethnobotanical and medicinal importance. This chapter deals with phytochemical composition, antioxidant, and antigenotoxic properties of these six Zingiberaceous plant extracts.

Phytochemistry and Antigenotoxic Properties of Six Ethnobotanically Important Members From the Family Zingiberaceae

2020 ◽  
pp. 131-153
Author(s):  
Anish Nag
Keyword(s):  
Antioxidant Properties ◽  
Zingiber Officinale ◽  
Dna Strand Breaks ◽  
Herbal Extracts ◽  
Strand Breaks ◽  
Phytochemical Composition ◽  
Curcuma Amada ◽  
Dna Damaging Agents ◽  
The Family ◽  
Dna Strand

Genotoxicity is considered as a potential cause of various diseases including cancer. During the last decade, herbal extracts attained a great deal of attention due to its safe and effective applications against various DNA damaging agents. However, the mechanism of DNA strand breaks by various mutagens and genotoxins is often correlated with the generation of Reactive Oxygen Species (ROS). Herbal extracts constitute a number of phytochemicals and those are reported to have considerable antioxidant properties, which are in turn capable of neutralizing ROS mediated DNA damage. The botanical family Zingiberaceae is reported to have significant antioxidant and antigenotoxic potential by various researchers. Among a number of species belonging to this family, six species, namely Alpinia galanga, A. zerumbet, Curcuma amada, C. caesia, Zingiber officinale, and Z. zerumbet, attract notable attention due to their remarkable ethnobotanical and medicinal importance. This chapter deals with phytochemical composition, antioxidant, and antigenotoxic properties of these six Zingiberaceous plant extracts.

scholarly journals DNA strand breaks: the DNA template alterations that trigger p53-dependent DNA damage response pathways.

1994 ◽  
Vol 14 (3) ◽  
pp. 1815-1823 ◽  
Author(s):  
W G Nelson ◽  
M B Kastan
Keyword(s):  
Excision Repair ◽  
P53 Protein ◽  
Dna Strand Breaks ◽  
Wild Type ◽  
Strand Breaks ◽  
Protein Levels ◽  
Dna Damaging Agents ◽  
Wild Type P53 ◽  
Dna Strand ◽  
Dna Template

The tumor suppressor protein p53 serves as a critical regulator of a G1 cell cycle checkpoint and of apoptosis following exposure of cells to DNA-damaging agents. The mechanism by which DNA-damaging agents elevate p53 protein levels to trigger G1/S arrest or cell death remains to be elucidated. In fact, whether damage to the DNA template itself participates in transducing the signal leading to p53 induction has not yet been demonstrated. We exposed human cell lines containing wild-type p53 alleles to several different DNA-damaging agents and found that agents which rapidly induce DNA strand breaks, such as ionizing radiation, bleomycin, and DNA topoisomerase-targeted drugs, rapidly triggered p53 protein elevations. In addition, we determined that camptothecin-stimulated trapping of topoisomerase I-DNA complexes was not sufficient to elevate p53 protein levels; rather, replication-associated DNA strand breaks were required. Furthermore, treatment of cells with the antimetabolite N(phosphonoacetyl)-L-aspartate (PALA) did not cause rapid p53 protein increases but resulted in delayed increases in p53 protein levels temporally correlated with the appearance of DNA strand breaks. Finally, we concluded that DNA strand breaks were sufficient for initiating p53-dependent signal transduction after finding that introduction of nucleases into cells by electroporation stimulated rapid p53 protein elevations. While DNA strand breaks appeared to be capable of triggering p53 induction, DNA lesions other than strand breaks did not. Exposure of normal cells and excision repair-deficient xeroderma pigmentosum cells to low doses of UV light, under conditions in which thymine dimers appear but DNA replication-associated strand breaks were prevented, resulted in p53 induction attributable to DNA strand breaks associated with excision repair. Our data indicate that DNA strand breaks are sufficient and probably necessary for p53 induction in cells with wild-type p53 alleles exposed to DNA-damaging agents.

scholarly journals Repair of DNA Strand Breaks by the Overlapping Functions of Lesion-Specific and Non-Lesion-Specific DNA 3′ Phosphatases

2001 ◽  
Vol 21 (21) ◽  
pp. 7191-7198 ◽  
Author(s):  
John R. Vance ◽  
Thomas E. Wilson
Keyword(s):  
Dna Damage ◽  
Oxidative Dna Damage ◽  
Synthetic Lethality ◽  
Dna Strand Breaks ◽  
Triple Mutant ◽  
Phosphatase Domain ◽  
Strand Breaks ◽  
Alternative Pathways ◽  
Processing Enzymes ◽  
Dna Strand

ABSTRACT In Saccharomyces cerevisiae, the apurinic/apyrimidinic (AP) endonucleases Apn1 and Apn2 act as alternative pathways for the removal of various 3′-terminal blocking lesions from DNA strand breaks and in the repair of abasic sites, which both result from oxidative DNA damage. Here we demonstrate that Tpp1, a homologue of the 3′ phosphatase domain of polynucleotide kinase, is a third member of this group of redundant 3′ processing enzymes. Unlike Apn1 and Apn2, Tpp1 is specific for the removal of 3′ phosphates at strand breaks and does not possess more general 3′ phosphodiesterase, exonuclease, or AP endonuclease activities. Deletion ofTPP1 in an apn1 apn2 mutant background dramatically increased the sensitivity of the double mutant to DNA damage caused by H2O2 and bleomycin but not to damage caused by methyl methanesulfonate. The triple mutant was also deficient in the repair of 3′ phosphate lesions left by Tdp1-mediated cleavage of camptothecin-stabilized Top1-DNA covalent complexes. Finally, the tpp1 apn1 apn2 triple mutation displayed synthetic lethality in combination with rad52, possibly implicating postreplication repair in the removal of unrepaired 3′-terminal lesions resulting from endogenous damage. Taken together, these results demonstrate a clear role for the lesion-specific enzyme, Tpp1, in the repair of a subset of DNA strand breaks.

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