Effects of 4-nonylphenol on oxidant/antioxidant balance system inducing hepatic steatosis in male rat

Kourouma, Ansoumane; Keita, Hady; Duan, Peng; Quan, Chao; Bilivogui, Koikoi Kebe; Qi, Suqin; Christiane, Ndjiembi Adjonga; Osamuyimen, Aidogie; Yang, Kecheng

doi:10.1016/j.toxrep.2015.10.006

Cited by 37 publications

(12 citation statements)

References 60 publications

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“…Linking the association with NAFLD described above, increased generation of ROS can induce inflammation in liver cells through lipid peroxidation (Day, 2002), and induces fat accumulation by inhibiting hepatocytes from secreting very low density lipoprotein (VLDL) (Polimeni et al, 2015). Analysis of the DE gene signatures unique to exposure to NP identified changes relating to the metabolism of ROS that in combination with changes in inflammation and fatty acid metabolism support previous studies suggesting NP has a role in the development of NAFLD (Kourouma et al, 2015).…”

Section: Non-estrogenic Effects Of Np Suggest Changes In Cell Death Asupporting

confidence: 70%

Systems analysis of the liver transcriptome in adult male zebrafish exposed to the non-ionic surfactant nonylphenol

Huff

Silveira

Hazard

et al. 2019

General and Comparative Endocrinology

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Nonylphenol (NP) arises from the environmental degradation of nonylphenol ethoxylates. It is a ubiquitous environmental contaminant and has been detected at levels up to 167 nM in rivers in the United States. NP is an endocrine disruptor (ED) that can act as an agonist for estrogen receptors. The Adverse Outcome Pathway (AOP) framework defines an adverse outcome as the causal result of a series of molecular initiating events (MIEs) and key events (KEs) that lead to altered phenotypes. This study examined the liver transcriptome after a 21 day exposure to NP and 17β-estradiol (E2) by exploiting the zebrafish (Danio rerio) as a systems toxicology model. The goal of this study was to tease out non-estrogenic genomic signatures associated with NP exposure using DNA microarray and RNA sequencing. Our experimental design included E2 as a positive and potent estrogenic control in order to effectively compare and contrast the 2 compounds. This approach allowed us to identify hepatic transcriptomic perturbations that could serve as MIEs for adverse health outcomes in response to NP. Our results revealed that exposure to NP was associated with differential expression (DE) of genes associated with the development of steatosis, disruption of metabolism, altered immune response, and metabolism of reactive oxygen species, further highlighting NP as a chemical of emerging concern (CEC).

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Section: Non-estrogenic Effects Of Np Suggest Changes In Cell Death Asupporting

confidence: 70%

Systems analysis of the liver transcriptome in adult male zebrafish exposed to the non-ionic surfactant nonylphenol

Huff

Silveira

Hazard

et al. 2019

General and Comparative Endocrinology

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“…In the view of TAC, TPX and MDA analysis in the blood lysate, NP challenged fish suffered from oxidative damage as consistent with other investigators (Solé, Fortuny, & Mañanós, ; Wu, Xu, Shen, Qiu, & Yang, ). Mounting evidences indicated shift of redox state towards pro‐oxidant side under NP stress by induction of reactive oxygen species formation, depletion of enzymatic and non‐enzymatic antioxidants, and upregulation of oxidative stress‐related genes (Kourouma et al., ; Park, ; Zhang, Yang, Cai, & Xu, ). It was supposed that NP‐associated haematotoxicity is secondary to devastated attack of reactive oxidant that overwhelmed antioxidant defence system.…”

Section: Discussionmentioning

confidence: 99%

Nigella sativa seed protects against 4-nonylphenol-induced haematotoxicity in Clarias gariepinus (Burchell, 1822): Oxidant/antioxidant rebalance

2017

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4-Nonylphenol (NP) is an emerging concern contaminant which is widely spread in the aquatic ecosystem. Nigella sativa seed (NSS) has multifaceted therapeutic values. This study aimed to give insight into the potential protective effect of NSS on NP-induced haematotoxicity in Clarias gariepinus through evaluation of haematological parameters, oxidant/antioxidant balance of blood lysate and histopathological investigation of blood smear. One hundred and fifty fish were divided into five groups (30/group). First group served as control which did not received NP exposure and fed basal diet without NSS supplementation. The other four groups were exposed to NP at a dose of 0.1 mg L −1 and fed diets supplemented with NSS at levels of 0, 10, 25 and 50 g/kg diet, respectively. Macrocytic hypochromic anaemia, thrombocytopenia, leucopenia, neutrophilia, lymphopenia, monocytosis and eosinophilia were observed following NP exposure together with increase in morphological erythrocyte alterations and micronuclei formation. Elevation in total peroxide and malondialdehyde and depletion in total antioxidant capacity of blood lysate were reported. We concluded that supplementation of NSS markedly ameliorated the previously listed manifestations, and the most effective doses were 25 and 50 g/kg feed.

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“…It should be noted that the impairment of mitochondrial activity was related to IR and obesity onset; thus, mitochondrial dysfunction induced by BPA may favor the development of NAFLD [ 108 ]. Similarly, other EDCs such as NP can exert significant effects on MMP loss and apoptosis of rat hepatocytes by promoting an increase in uncoupling protein-2 (UCP2) [ 109 ], deregulating Bax/Bcl-2 activity, and triggering mRNA activation of TNF-α, caspase-9, and Fas/FasL [ 110 ], thus promoting the development of mitochondrial dysfunction, liver injury, and steatosis.…”

Section: Mechanisms Of Action Of Endocrine-disrupting Chemicals In Nafldmentioning

confidence: 99%

Role of Endocrine-Disrupting Chemicals in the Pathogenesis of Non-Alcoholic Fatty Liver Disease: A Comprehensive Review

Cano

Pérez

Angarita

et al. 2021

IJMS

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Non-alcoholic fatty liver disease (NAFLD) is considered the most common liver disorder, affecting around 25% of the population worldwide. It is a complex disease spectrum, closely linked with other conditions such as obesity, insulin resistance, type 2 diabetes mellitus, and metabolic syndrome, which may increase liver-related mortality. In light of this, numerous efforts have been carried out in recent years in order to clarify its pathogenesis and create new prevention strategies. Currently, the essential role of environmental pollutants in NAFLD development is recognized. Particularly, endocrine-disrupting chemicals (EDCs) have a notable influence. EDCs can be classified as natural (phytoestrogens, genistein, and coumestrol) or synthetic, and the latter ones can be further subdivided into industrial (dioxins, polychlorinated biphenyls, and alkylphenols), agricultural (pesticides, insecticides, herbicides, and fungicides), residential (phthalates, polybrominated biphenyls, and bisphenol A), and pharmaceutical (parabens). Several experimental models have proposed a mechanism involving this group of substances with the disruption of hepatic metabolism, which promotes NAFLD. These include an imbalance between lipid influx/efflux in the liver, mitochondrial dysfunction, liver inflammation, and epigenetic reprogramming. It can be concluded that exposure to EDCs might play a crucial role in NAFLD initiation and evolution. However, further investigations supporting these effects in humans are required.

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Effects of 4-nonylphenol on oxidant/antioxidant balance system inducing hepatic steatosis in male rat

Cited by 37 publications

References 60 publications

Systems analysis of the liver transcriptome in adult male zebrafish exposed to the non-ionic surfactant nonylphenol

Systems analysis of the liver transcriptome in adult male zebrafish exposed to the non-ionic surfactant nonylphenol

Nigella sativa seed protects against 4-nonylphenol-induced haematotoxicity in Clarias gariepinus (Burchell, 1822): Oxidant/antioxidant rebalance

Role of Endocrine-Disrupting Chemicals in the Pathogenesis of Non-Alcoholic Fatty Liver Disease: A Comprehensive Review

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