Aflatoxin B1 impairs leydig cells through inhibiting AMPK/mTOR-mediated autophagy flux pathway

Chen, Xianwu; Li, Chao; Chen, Yong; Ni, Chaobo; Chen, Xiuxiu; Zhang, Linlei; Xu, Xuni; Chen, Min; Ma, Xinyi; Zhan, Hui-lu; Xu, Aidong; Ge, Ren‐Shan; Guo, Xiaoling

doi:10.1016/j.chemosphere.2019.05.273

Cited by 52 publications

(55 citation statements)

References 54 publications

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“…16,17 Elucidated mechanisms associated with AFB1-mediated reproductive toxicity include suppression of androgen biosynthetic proteins (17 β-hydroxysteroid dehydrogenase 3, 3β-hydroxysteroid dehydrogenase, and steroidogenic acute regulator), induction of oxidative stress, inhibition of antioxidant defense systems, germ cell apoptosis and autophagy. 18–20 Thus, the potential chemopreventive or chemotherapeutic agents to assuage the deleterious effects of AFB1 in the exposed population are warranted.…”

Section: Introductionmentioning

confidence: 99%

Gallic acid enhances reproductive function by modulating oxido-inflammatory and apoptosis mediators in rats exposed to aflatoxin-B1

Owumi

Adedara

Akomolafe

et al. 2020

Exp Biol Med (Maywood)

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Aflatoxin B1 (AFB1) is reported to elicit adverse reproductive outcomes in animals. Gallic acid (GA) is known to exhibit antioxidant and inflammatory bioactivities. The impact of GA on AFB1-facilitated reproductive dysfunction is nonexistent in literature. This investigation elucidated GA protective effect on AFB1-induced reproductive toxicities in rats, exposed for 28 consecutive days to AFB1 (75 µg/kg), or co-treated with GA (20 or 40 mg/kg) body weight. AFB1 significantly (p < 0.05) reduced testicular function biomarkers, serum hormonal levels, and functional sperm characteristics in experimental animals. GA abated AFB1-induced increases (p < 0.05) in lipid peroxidation and reactive oxygen and nitrogen species, suppressed myeloperoxidase, interleukin-1β, nitric oxide, and tumor necrosis factor-α levels—inflammatory biomarkers—in testes, epididymis, and hypothalamus. Furthermore, GA improved antioxidant defenses and alleviated reduction in interleukin-10, caspase-3 activation, and histological variations in epididymis, testes, and hypothalamus of rats dosed with AFB1. Conclusively, GA enhanced reproductive function in AFB1-exposed rats by modulating inflammatory, oxidative stress, and apoptosis mediators. Impact statement Infertility resulting from reproductive deficiency can be stressful. Exposure to aflatoxin B1, a dietary mycotoxin prevalent in improperly stored grains, is reported to elicit reproductive insufficiencies and infertility. We, therefore, examined the likely beneficial effect of gallic acid (GA) a phytochemical, recognized to exhibit in vitro and in vivo pharmacological bioactivities against oxidative stress and related inflammatory damages in rats, since AFB1 toxicities are predicated on oxidative epoxide formation, in a bid to proffer new evidence to advance the field of nutriceutical application from plant-derived chemopreventive agents. Our findings will advance the field of chemoprevention by presenting data absent in the literature on GA. Our results demonstrate further evidence for GA conferred protection against AFB1-mediated histological lesions in testes, epididymis, and hypothalamus of treated rats; suppresses oxidative damages, relieved inflammatory and apoptotic responses, restored sperm functional characteristics, and hormonal levels relevant for reproductive integrity and function.

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Section: Introductionmentioning

confidence: 99%

Gallic acid enhances reproductive function by modulating oxido-inflammatory and apoptosis mediators in rats exposed to aflatoxin-B1

Owumi

Adedara

Akomolafe

et al. 2020

Exp Biol Med (Maywood)

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“…The decreased levels of pAMPK/AMPK ratio in the exercised group suggest enhanced gluconeogenesis, which promotes generation of glucose from various sources such as tryglycerides, proteins, and lactate. Decreased pAMPK/AMPK levels and an increased pmTOR/mTOR ratio, could mean increased levels of apoptosis in the liver (Chen et al 2019 ). However, in our case, the pmTOR/mTOR ratio in the exercise trained transgenic animals was decreased, albeit not significantly, compared to the control group.…”

Section: Discussionmentioning

confidence: 99%

Exercise combined with a probiotics treatment alters the microbiome, but moderately affects signalling pathways in the liver of male APP/PS1 transgenic mice

et al. 2020

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It has been demonstrated that physical exercise and probiotic supplementation delay the progress of Alzheimer’s Disease (AD) in male APP/PS1TG mice. However, it has also been suggested that both exercise and AD have systemic effects. We have studied the effects of exercise training and probiotic treatment on microbiome and biochemical signalling proteins in the liver. The results suggest that liver is under oxidative stress, since SOD2 levels of APP/PS1 mice were decreased when compared to a wild type of mice. Exercise training prevented this decrease. We did not find significant changes in COX4, SIRT3, PGC-1a or GLUT4 levels, while the changes in pAMPK/AMPK, pmTOR/mTOR, pS6/S6 and NRF2 levels were randomly modulated. The data suggest that exercise and probiotics-induced changes in microbiome do not strongly affect mitochondrial density or protein synthesis-related AMPK/mTOR/S6 pathways in the liver of these animals.

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“…In a study by Li et al, the dietary 0.6 mg•kg −1 of AFB1 inhibited chicken spleen growth via G 0 /G 1 cell-cycle arrest, as well as reduced mRNA expression of cyclin D1 and elevated CDK6, p21/53 and ATM expression, suggesting that AFB1 induced G 0 G 1 phase arrest through activated ATM-p53-p21-cyclin D/CDK6 route in the splenocytes [159]. Chen et al investigated whether the toxicity of AFB1 on Leydig cells could be attributed to the enhancement of ROS generation, the prevention of T-biosynthesis gene expression, the reduction in Leydig cell count, and induction of cell apoptosis via AMPK/mTOR-mediated suppression of autophagic flux [160]. In an in vitro study, Liu et al, reported genotoxic impacts induced by AFB1 and MC-LR combinative exposure in hepatocytes through oxidative stress and DNA base excision repair genes [161].…”

Section: Toxicity and Health Impacts Of Aflatoxinsmentioning

confidence: 99%

Characteristics, Occurrence, Detection and Detoxification of Aflatoxins in Foods and Feeds

Nazhand

Durazzo²,

Lucarini³

et al. 2020

Foods

106

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Mycotoxin contamination continues to be a food safety concern globally, with the most toxic being aflatoxins. On-farm aflatoxins, during food transit or storage, directly or indirectly result in the contamination of foods, which affects the liver, immune system and reproduction after infiltration into human beings and animals. There are numerous reports on aflatoxins focusing on achieving appropriate methods for quantification, precise detection and control in order to ensure consumer safety. In 2012, the International Agency for Research on Cancer (IARC) classified aflatoxins B1, B2, G1, G2, M1 and M2 as group 1 carcinogenic substances, which are a global human health concern. Consequently, this review article addresses aflatoxin chemical properties and biosynthetic processes; aflatoxin contamination in foods and feeds; health effects in human beings and animals due to aflatoxin exposure, as well as aflatoxin detection and detoxification methods.

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Aflatoxin B1 impairs leydig cells through inhibiting AMPK/mTOR-mediated autophagy flux pathway

Cited by 52 publications

References 54 publications

Gallic acid enhances reproductive function by modulating oxido-inflammatory and apoptosis mediators in rats exposed to aflatoxin-B1

Gallic acid enhances reproductive function by modulating oxido-inflammatory and apoptosis mediators in rats exposed to aflatoxin-B1

Exercise combined with a probiotics treatment alters the microbiome, but moderately affects signalling pathways in the liver of male APP/PS1 transgenic mice

Characteristics, Occurrence, Detection and Detoxification of Aflatoxins in Foods and Feeds

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