Selenium Yeast Alleviates Ochratoxin A-Induced Hepatotoxicity via Modulation of the PI3K/AKT and Nrf2/Keap1 Signaling Pathways in Chickens

Kang, Li; Chao, Zou; Cui, Tong; Sun, Lin; Cao, Zhongjun; Yang, Shuai; Lyu, Qiufeng

doi:10.3390/toxins12030143

Cited by 42 publications

(29 citation statements)

References 49 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…A recent study revealed that AFB 1 -induced liver damage in broiler chicks has been associated with dysregulating the Nrf2 signaling pathway [ 13 ]. Therefore, Nrf2 signaling is regarded as the most significant therapeutic target for preventing and treating oxidative stress-induced liver damage [ 24 , 25 ]. Although, a study reported that luteolin has a therapeutic impact on ochratoxin A-induced oxidative injury in NRK-52E kidney cells [ 17 ].…”

Section: Introductionmentioning

confidence: 99%

Luteolin Alleviates AflatoxinB1-Induced Apoptosis and Oxidative Stress in the Liver of Mice through Activation of Nrf2 Signaling Pathway

Rajput

Shaukat

et al. 2021

Antioxidants

View full text Add to dashboard Cite

Aflatoxin B1 (AFB1), a threatening mycotoxin, usually provokes oxidative stress and causes hepatotoxicity in animals and humans. Luteolin (LUTN), well-known as an active phytochemical agent, acts as a strong antioxidant. This research was designed to investigate whether LUTN exerts protective effects against AFB1-induced hepatotoxicity and explore the possible molecular mechanism in mice. A total of forty-eight mice were randomly allocated following four treatment groups (n = 12): Group 1, physiological saline (CON). Group 2, treated with 0.75 mg/kg BW aflatoxin B1 (AFB1). Group 3, treated with 50 mg/kg BW luteolin (LUTN), and Group 4, treated with 0.75 mg/kg BW aflatoxin B1 + 50 mg/kg BW luteolin (AFB1 + LUTN). Our findings revealed that LUTN treatment significantly alleviated growth retardation and rescued liver injury by relieving the pathological and serum biochemical alterations (ALT, AST, ALP, and GGT) under AFB1 exposure. LUTN ameliorated AFB1-induced oxidative stress by scavenging ROS and MDA accumulation and boosting the capacity of the antioxidant enzyme (CAT, T-SOD, GSH-Px and T-AOC). Moreover, LUTN treatment considerably attenuates the AFB1-induced apoptosis in mouse liver, as demonstrated by declined apoptotic cells percentage, decreased Bax, Cyt-c, caspase-3 and caspase-9 transcription and protein with increased Bcl-2 expression. Notably, administration of LUTN up-regulated the Nrf2 and its associated downstream molecules (HO-1, NQO1, GCLC, SOD1) at mRNA and protein levels under AFB1 exposure. Our results indicated that LUTN effectively alleviated AFB1-induced liver injury, and the underlying mechanisms were associated with the activation of the Nrf2 signaling pathway. Taken together, LUTN may serve as a potential mitigator against AFB1-induced liver injury and could be helpful for the development of novel treatment to combat liver diseases in humans and/or animals.

show abstract

Section: Introductionmentioning

confidence: 99%

Luteolin Alleviates AflatoxinB1-Induced Apoptosis and Oxidative Stress in the Liver of Mice through Activation of Nrf2 Signaling Pathway

Rajput

Shaukat

et al. 2021

Antioxidants

View full text Add to dashboard Cite

show abstract

“…OTA contamination in feed seriously affects the health and production performance of animals, which may also harm people through the food chain. Numerous studies have reported that OTA has renal toxicity, liver toxicity, and carcinogenic and teratogenic effects [ 7 , 8 , 9 , 10 ]. In recent years, biodegradation strategies for OTA detoxification have become a promising method.…”

Section: Discussionmentioning

confidence: 99%

“…The target organs of OTA are considered to be the kidney and liver. Studies have reported that OTA causes nephrotoxicity, hepatotoxicity, immunotoxicity, teratogenicity, genotoxicity, and carcinogenicity in animals [ 7 , 8 , 9 , 10 ]. Plenty of animal feeding trials have been performed to evaluate the potential toxicity of OTA.…”

Section: Introductionmentioning

confidence: 99%

Bacillus subtilis ANSB168 Producing d-alanyl-d-alanine Carboxypeptidase Could Alleviate the Immune Injury and Inflammation Induced by Ochratoxin A

Qing

Huo

Huang

et al. 2021

IJMS

View full text Add to dashboard Cite

Ochratoxin A (OTA) is toxic to animals and threatens food safety through residues in animal tissues. A novel degrading strain Bacillus subtilis ANSB168 was isolated and further investigated. We cloned d-alanyl-d-alanine carboxypeptidase DacA and DacB from ANSB168 and over-expressed them in Escherichia coli Rosetta (DE3). Then, we characterized the OTA degradation mechanism of DacA and DacB, which was degrading OTA into OTα. A total of 45 laying hens were divided into three equal groups. The control group was fed basal feed, and other groups were administered with OTA (250 μg/kg of feed). A freeze-dried culture powder of ANSB168 (3 × 107 CFU/g, 2 kg/T of feed) was added to one of the OTA-fed groups for 28 days from day one of the experiment. We found that OTA significantly damaged the kidney and liver, inducing inflammation and activating the humoral immune system, causing oxidative stress in the layers. The ANSB168 bioproduct was able to alleviate OTA-induced kidney and liver damage, relieving OTA-induced inflammation and oxidative stress. Overall, DacA and DacB derived from ANSB168 degraded OTA into OTα, while the ANSB168 bioproduct was able to alleviate damages induced by OTA in laying hens.

show abstract

“…Flavonoid luteolin regulates Nrf2 and HIF-1α signalling pathways to alleviate OTA-induced oxidative stress (Liu et al 2020 ). Carotenoid astaxanthin similarly to luteolin protects against OTA-induced kidney injury (Li et al 2020b ), similarly to yeast selenium used as diet supplement (Li et al 2020c ). Also quercetin, a natural flavanol, stimulates translocation of Nrf2 to the nucleus and increases its expression after cell exposure to OTA and thus alleviate the toxicity of this mycotoxin (Ramyaa and Padma 2013 ; Ramyaa et al 2014 ).…”

Section: Natural Antioxidantsmentioning

confidence: 99%

Nrf2: a main responsive element in cells to mycotoxin-induced toxicity

Kozieł

Kowalska

Piastowska-Ciesielska

2021

Arch Toxicol

View full text Add to dashboard Cite

Nuclear factor erythroid 2-like 2 (Nrf2) is a transcription factor participating in response to cellular oxidative stress to maintain the redox balance. Generation of reactive oxygen species (ROS) and, in consequence, oxidative stress, are physiological as well as pathological processes which take place in almost all types of cells. Nrf2, in response to oxidative stress, activates expression and production of antioxidant enzymes to remove free radicals. However, the role of Nrf2 seems to be more sophisticated and its increased expression observed in cancer cells allows to draw a conclusion that its role is tissue—and condition—dependent. Interestingly, Nrf2 might also play a crucial role in response to environmental factors like mycotoxins. Thus, the aim of the study is to review the role of Nrf2 in cells exposed to most common mycotoxins to check if the Nrf2 signaling pathway serves as the main response element to mycotoxin-induced oxidative stress in human and animal cells and if it can be a target of detoxifying agents.

show abstract

Selenium Yeast Alleviates Ochratoxin A-Induced Hepatotoxicity via Modulation of the PI3K/AKT and Nrf2/Keap1 Signaling Pathways in Chickens

Cited by 42 publications

References 49 publications

Luteolin Alleviates AflatoxinB1-Induced Apoptosis and Oxidative Stress in the Liver of Mice through Activation of Nrf2 Signaling Pathway

Luteolin Alleviates AflatoxinB1-Induced Apoptosis and Oxidative Stress in the Liver of Mice through Activation of Nrf2 Signaling Pathway

Bacillus subtilis ANSB168 Producing d-alanyl-d-alanine Carboxypeptidase Could Alleviate the Immune Injury and Inflammation Induced by Ochratoxin A

Nrf2: a main responsive element in cells to mycotoxin-induced toxicity

Contact Info

Product

Resources

About