Catechin from green tea had the potential to decrease the chlorpyrifos induced oxidative stress in larval zebrafish (Danio rerio)

Author(s):  
Yun Zhao ◽  
Chanlin Fang ◽  
Cuiyuan Jin ◽  
Zhiwei Bao ◽  
Guiling Yang ◽  
...  
Chemosphere ◽  
2020 ◽  
Vol 241 ◽  
pp. 125129 ◽  
Author(s):  
Shuying Li ◽  
Yao Jiang ◽  
Qianqian Sun ◽  
Scott Coffin ◽  
Lili Chen ◽  
...  

2021 ◽  
Author(s):  
Dong Seok Lim ◽  
Seo Yeong Kim ◽  
Seo Young Jun ◽  
Eun Jin Choi ◽  
Seok Woo Ko ◽  
...  

Abstract Background Exposure to oxidative stress (OS) incurs various consequences in animals’ life from molecular to organismic level. Survival and social affinity are the two representative fitness components of animals that can be impacted by early exposure to OS during the developmental process. However, the effect of early OS exposure on survival and social affinity has not been well addressed. Results In this study, we treated 0, 1, and 5 mM of hydrogen peroxide solution to four-days post fertilization (dpf) larval zebrafish (Danio rerio) for 30 mins, and examined their survival until 19 dpf and social affinity at 28 dpf. There were no significant differences in survival among the treatment groups. On the other hand, social affinity was reduced in the individuals exposed to 5 mM hydrogen peroxide solution. All the groups demonstrated a similar level of locomotion. Conclusions These findings indicate that mild neonatal OS exposure did not affect the survival but partially hampered social affinity. Whether and how partially hampered social affinity in larval zebrafish persists to adulthood need to be investigated.


2020 ◽  
Vol 227 ◽  
pp. 105607
Author(s):  
Andrew Kataba ◽  
Tarryn L. Botha ◽  
Shouta M.M. Nakayama ◽  
Yared B. Yohannes ◽  
Yoshinori Ikenaka ◽  
...  

2008 ◽  
Vol 4 (4) ◽  
pp. 365-370 ◽  
Author(s):  
S. Ounjaijean ◽  
C. Thephinlap ◽  
U. Khansuwan ◽  
C. Phisalapong ◽  
S. Fucharoen ◽  
...  

Antioxidants ◽  
2021 ◽  
Vol 10 (7) ◽  
pp. 1076
Author(s):  
Guoyi Tang ◽  
Yu Xu ◽  
Cheng Zhang ◽  
Ning Wang ◽  
Huabin Li ◽  
...  

Nonalcoholic fatty liver diseases (NAFLD) represent a set of liver disorders progressing from steatosis to steatohepatitis, fibrosis, cirrhosis, and hepatocellular carcinoma, which induce huge burden to human health. Many pathophysiological factors are considered to influence NAFLD in a parallel pattern, involving insulin resistance, oxidative stress, lipotoxicity, mitochondrial dysfunction, endoplasmic reticulum stress, inflammatory cascades, fibrogenic reaction, etc. However, the underlying mechanisms, including those that induce NAFLD development, have not been fully understood. Specifically, oxidative stress, mainly mediated by excessive accumulation of reactive oxygen species, has participated in the multiple NAFLD-related signaling by serving as an accelerator. Ameliorating oxidative stress and maintaining redox homeostasis may be a promising approach for the management of NAFLD. Green tea is one of the most important dietary resources of natural antioxidants, above which epigallocatechin gallate (EGCG) notably contributes to its antioxidative action. Accumulative evidence from randomized clinical trials, systematic reviews, and meta-analysis has revealed the beneficial functions of green tea and EGCG in preventing and managing NAFLD, with acceptable safety in the patients. Abundant animal and cellular studies have demonstrated that green tea and EGCG may protect against NAFLD initiation and development by alleviating oxidative stress and the related metabolism dysfunction, inflammation, fibrosis, and tumorigenesis. The targeted signaling pathways may include, but are not limited to, NRF2, AMPK, SIRT1, NF-κB, TLR4/MYD88, TGF-β/SMAD, and PI3K/Akt/FoxO1, etc. In this review, we thoroughly discuss the oxidative stress-related mechanisms involved in NAFLD development, as well as summarize the protective effects and underlying mechanisms of green tea and EGCG against NAFLD.


2009 ◽  
Vol 297 (2) ◽  
pp. R412-R420 ◽  
Author(s):  
Shelby L. Steele ◽  
Kwok Hong Andy Lo ◽  
Vincent Wai Tsun Li ◽  
Shuk Han Cheng ◽  
Marc Ekker ◽  
...  

Fish exposed to hypoxia develop decreased heart rate, or bradycardia, the physiological significance of which remains unknown. The general muscarinic receptor antagonist atropine abolishes the development of this hypoxic bradycardia, suggesting the involvement of muscarinic receptors. In this study, we tested the hypothesis that the hypoxic bradycardia is mediated specifically by stimulation of the M2 muscarinic receptor, the most abundant subtype in the vertebrate heart. Zebrafish ( Danio rerio) were reared at two levels of hypoxia (30 and 40 Torr Po2) from the point of fertilization. In hypoxic fish, the heart rate was significantly lower than in normoxic controls from 2 to 10 days postfertilization (dpf). At the more severe level of hypoxia (30 Torr Po2), there were significant increases in the relative mRNA expression of M 2 and the cardiac type β-adrenergic receptors ( β1AR, β2aAR, and β2bAR) at 4 dpf. The hypoxic bradycardia was abolished (at 40 Torr Po2) or significantly attenuated (at 30 Torr Po2) in larvae experiencing M2 receptor knockdown (using morpholino antisense oligonucleotides). Sham-injected larvae exhibited typical hypoxic bradycardia in both hypoxic regimens. The expression of β1AR, β2aAR, β2bAR, and M 2 mRNA was altered at various stages between 1 and 4 dpf in larvae experiencing M2 receptor knockdown. Interestingly, M2 receptor knockdown revealed a cardioinhibitory role for the β2-adrenergic receptor. This is the first study to demonstrate a specific role of the M2 muscarinic receptor in the initiation of hypoxic bradycardia in fish.


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