2018
DOI: 10.1016/j.dnarep.2018.07.003
|View full text |Cite
|
Sign up to set email alerts
|

DNA damage and oxidative stress in long-lived aquatic organisms

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
2
2

Citation Types

0
7
0

Year Published

2020
2020
2024
2024

Publication Types

Select...
8
1
1

Relationship

0
10

Authors

Journals

citations
Cited by 17 publications
(9 citation statements)
references
References 144 publications
0
7
0
Order By: Relevance
“…Thus, it may impair fish health, antioxidant and immune responses. Excessive ROS can cause various tissue damages of fish, such as protein oxidation, lipid peroxidation and DNA damage (Wojtczyk‐Miaskowska & Schlichtholz, 2018). In the present study, fish farmed at HSD group exhibited lower hepatic SOD and CAT activities on 120 days.…”
Section: Discussionmentioning
confidence: 99%
“…Thus, it may impair fish health, antioxidant and immune responses. Excessive ROS can cause various tissue damages of fish, such as protein oxidation, lipid peroxidation and DNA damage (Wojtczyk‐Miaskowska & Schlichtholz, 2018). In the present study, fish farmed at HSD group exhibited lower hepatic SOD and CAT activities on 120 days.…”
Section: Discussionmentioning
confidence: 99%
“…Hormetic priming describes the beneficial effects of pre-exposure enhancing the ability to cope with subsequent encounters of similar or higher levels of stress later in life, as opposed to individuals without previous experience or primed under severe stress (Costantini, 2014). Mild oxidative stress presents a common source of hormetic priming (Costantini, 2014) and is a hypothesized driver of longevity (Ristow and Schmeisser, 2014;Wojtczyk-Miaskowska and Schlichtholz, 2018). For example, early-life exposure to moderate oxidative stress in the Caribbean fruit fly Anastrepha suspensa and zebra finch Taeniopygia guttata decreases cellular damage and increases proteomic defense, energy assimilation and survival under a subsequent stress encounter during adulthood (Costantini et al, 2012;Visser et al, 2018).…”
Section: Introductionmentioning
confidence: 99%
“…Similarly, our results showed that inhibition of survivin caused the increase of reactive oxygen species (ROS) level; therefore, high levels of ROS might be one of the causes that contribute to early embryonic dysplasia after inhibition of survivin activity. It is well known that ROS could induce DNA damage and consequently, a DNA damage response (DDR) [33,34]. ROS could induce double-strand DNA breaks (DSBs) and oxidative clustered DNA lesions (OCDLs) [35].…”
Section: Discussionmentioning
confidence: 99%