Protective effects of some bioactive phenolic compounds against DNA adduct formation and interstrand cross-links caused by reactive carbonyl species in chemical models

2011 ◽  
Author(s):  
Tsz-kin, James To
2019 ◽  
Vol 10 ◽  
Author(s):  
Jun’ichi Mano ◽  
Sayaka Kanameda ◽  
Rika Kuramitsu ◽  
Nagisa Matsuura ◽  
Yasuo Yamauchi

Antioxidants ◽  
2021 ◽  
Vol 10 (5) ◽  
pp. 690
Author(s):  
Giancarlo Aldini ◽  
Alessandra A. Altomare

The Special issue is composed of 13 contributions: 9 research papers and 4 reviews [...]


Molecules ◽  
2016 ◽  
Vol 21 (3) ◽  
pp. 280 ◽  
Author(s):  
Sung Hwang ◽  
Yoon-Mi Lee ◽  
Giancarlo Aldini ◽  
Kyung-Jin Yeum

Antioxidants ◽  
2020 ◽  
Vol 9 (5) ◽  
pp. 446
Author(s):  
Seung-Cheol Jee ◽  
Min Kim ◽  
Kyeong Seok Kim ◽  
Hyung-Sik Kim ◽  
Jung-Suk Sung

Benzo[a]pyrene (B[a]P), a group 1 carcinogen, induces mutagenic DNA adducts. Myricetin is present in many natural foods with diverse biological activities, such as anti-oxidative and anti-cancer activities. The aim of this study was to investigate the protective effects of myricetin against B[a]P-induced toxicity. Treatment of B[a]P induced cytotoxicity on HepG2 cells, whereas co-treatment of myricetin with B[a]P reduced the formation of the B[a]P-7,8-dihydrodiol-9,10-epoxide (BPDE)-DNA adduct, which recovered cell viability. Furthermore, we found a protective effect of myricetin against B[a]P-induced genotoxicity in rats, via myricetin-induced inhibition of 8-hydroxy-2′-deoxyguanosine (8-OHdG) and BPDE-DNA adduct formation in the liver, kidney, colon, and stomach tissue. This inhibition was more prominent in the liver than in other tissues. Correspondingly, myricetin regulated the phase I and II enzymes that inhibit B[a]P metabolism and B[a]P metabolites conjugated with DNA by reducing and inducing CYP1A1 and glutathione S-transferase (GST) expression, respectively. Taken together, this showed that myricetin attenuated B[a]P-induced genotoxicity via regulation of phase I and II enzymes. Our results suggest that myricetin is anti-genotoxic, and prevents oxidative DNA damage and BPDE-DNA adduct formation via regulation of phase I and II enzymes.


Plants ◽  
2019 ◽  
Vol 8 (10) ◽  
pp. 391 ◽  
Author(s):  
Mano ◽  
Biswas ◽  
Sugimoto

As reactive oxygen species (ROS) play critical roles in plants to determine cell fate in various physiological situations, there is keen interest in the biochemical processes of ROS signal transmission. Reactive carbonyl species (RCS), the ,-unsaturated aldehydes and ketones produced from lipid peroxides, due to their chemical property to covalently modify protein, can mediate ROS signals to proteins. Comprehensive carbonyl analysis in plants has revealed that more than a dozen different RCS, e.g., acrolein, 4-hydroxy-(E)-2-nonenal and malondialdehyde, are produced from various membranes, and some of them increase and modify proteins in response to oxidative stimuli. At early stages of response, specific subsets of proteins are selectively modified with RCS. The involvement of RCS in ROS signaling can be judged on three criteria: (1) A stimulus to increase the ROS level in plants leads to the enhancement of RCS levels. (2) Suppression of the increase of RCS by scavenging enzymes or chemicals diminishes the ROS-induced response. (3) Addition of RCS to plants evokes responses similar to those induced by ROS. On these criteria, the RCS action as damaging/signaling agents has been demonstrated for root injury, programmed cell death, senescence of siliques, stomata response to abscisic acid, and root response to auxin. RCS thus act as damage/signal mediators downstream of ROS in a variety of physiological situations. A current picture and perspectives of RCS research are presented in this article.


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