10-Oxo-trans-11-octadecenoic acid generated from linoleic acid by a gut lactic acid bacterium Lactobacillus plantarum is cytoprotective against oxidative stress

Furumoto, Hidehiro; Nanthirudjanar, Tharnath; Kume, Toshiaki; Izumi, Yasukatsu; Park, Si‐Bum; Kitamura, Nahoko; Kishino, Shigenobu; Ogawa, Jun; Hirata, Takashi; Sugawara, Tatsuya

doi:10.1016/j.taap.2016.02.012

Cited by 48 publications

(46 citation statements)

References 49 publications

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“…Interestingly, Nrf2 mRNA and protein expressions were dose-dependently increased in HepG2 cells exposed to SA, OA, and ALA, but dose-dependently decreased in HepG2 cells exposed to LA, although still much higher than the control cells. The current reports showed that although LA and its metabolite derivatives play cytoprotective role in HepG2 cells and mouse/rat organs via inducing the expression of Nrf2 and its downstream antioxidative genes (Mollica et al, 2014; Furumoto et al, 2016), LA concentrations higher or lower than the optimal value attenuated its auxo-action on Nrf2 expression (Zeng et al, 2016). However, the exact mechanism of diverse LA concentrations (with similar cytotoxicity) showed different effects on inducing Nrf2 expression remains to be investigated.…”

Section: Discussionmentioning

confidence: 98%

High Fat Diet-Induced Hepatic 18-Carbon Fatty Acids Accumulation Up-Regulates CYP2A5/CYP2A6 via NF-E2-Related Factor 2

et al. 2017

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To investigate the role of hepatic 18-carbon fatty acids (FA) accumulation in regulating CYP2A5/2A6 and the significance of Nrf2 in the process during hepatocytes steatosis, Nrf2-null, and wild type mice fed with high-fat diet (HFD), and Nrf2 silenced or over expressed HepG2 cells administered with 18-carbon FA were used. HE and Oil Red O staining were used for mice hepatic pathological examination. The mRNA and protein expressions were measured with real-time PCR and Western blot. The results showed that hepatic CYP2A5 and Nrf2 expression levels were increased in HFD fed mice accompanied with hepatic 18-carbon FA accumulation. The Nrf2 expression was increased dose-dependently in cells administered with increasing concentrations of stearic acid, oleic acid, and alpha-linolenic acid. The Nrf2 expression was dose-dependently decreased in cells treated with increasing concentrations of linoleic acid, but the Nrf2 expression level was still found higher than the control cells. The CYP2A6 expression was increased dose-dependently in increasing 18-carbon FA treated cells. The HFD-induced up-regulation of hepatic CYP2A5 in vivo and the 18-carbon FA treatment induced up-regulation of CYP2A6 in HepG2 cells were, respectively, inhibited by Nrf2 deficiency and Nrf2 silencing. While the basal expression of mouse hepatic CYP2A5 was not impeded by Nrf2 deletion. Nrf2 over expression improved the up-regulation of CYP2A6 induced by 18-carbon FA. As the classical target gene of Nrf2, GSTA1 mRNA relative expression was increased in Nrf2 over expressed cells and was decreased in Nrf2 silenced cells. In presence or absence of 18-carbon FA treatment, the change of CYP2A6 expression level was similar to GSTA1 in Nrf2 silenced or over expressed HepG2 cells. It was concluded that HFD-induced hepatic 18-carbon FA accumulation contributes to the up-regulation of CYP2A5/2A6 via activating Nrf2. However, the CYP2A5/2A6 expression does not only depend on Nrf2.

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Section: Discussionmentioning

confidence: 98%

High Fat Diet-Induced Hepatic 18-Carbon Fatty Acids Accumulation Up-Regulates CYP2A5/CYP2A6 via NF-E2-Related Factor 2

et al. 2017

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“…107–113 These microbial metabolites may help preserve intestinal barrier integrity, reduce oxidative stress, and lower inflammation. 114, 115 Given that Lactobacillus is selectively enriched by omega-3 fatty acids, there may exist a reciprocal mechanism by which gut microbes adapt to host dietary change with functional consequences for host health. Moreover, a cross-feeding effect has been noted between human Bifidobacterium, which produces lactate and acetate, and the butyrate-producing species, such as Eubacterium rectale, which convert lactate to butyrate.…”

Section: Marine Omega-3 Fatty Acidsmentioning

confidence: 99%

Environmental Factors, Gut Microbiota, and Colorectal Cancer Prevention

Song

Chan

2019

Clinical Gastroenterology and Hepatology

246

157

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The substantial burden of colorectal cancer and increasing trend in young adults highlight the importance of lifestyle modification as a complement to screening for colorectal cancer prevention. Several dietary and lifestyle factors have been implicated in the development of colorectal cancer, possibly through the intricate metabolic and inflammatory mechanisms. Likewise, as a key metabolic and immune regulator, the gut microbiota has been recognized to play an important role in colorectal tumorigenesis. Increasing data support that environmental factors are crucial determinants for the gut microbial composition and function, whose alterations induce changes in the host gene expression, metabolic regulation, and local and systemic immune response, thereby influencing cancer development. Here, we review the epidemiologic and mechanistic evidence regarding the links between diet and lifestyle and the gut microbiota in the development of colorectal cancer. We focus on factors for which substantial data support their importance for colorectal cancer and their potential role in the gut microbiota, including overweight and obesity, physical activity, dietary patterns, fiber, red and processed meat, marine omega-3 fatty acid, alcohol, and smoking. We also briefly describe other colorectal cancer-preventive factors for which the links with the gut microbiota have been suggested but remain to be mechanistically characterized, including vitamin D status, dairy consumption, and metformin use. Given limitations in available evidence, we highlight the need for further investigations in the relationship between environmental factors, gut microbiota, and colorectal cancer, which may lead to development and clinical translation of potential microbiota-based strategies for cancer prevention.

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“…The metabolites of polyunsaturated fatty acids (PUFAs), in particular, electrophilic lipid oxidation and nitration products, can induce Nrf2 activation [25]. Recently, a linoleic acid derivative, 10-Oxo-trans-11-octadecenoic acid (KetoC) generated by Lactobacillus plantarum , a bacterial resident in the human gut, has been shown to be an activator of Nrf2-ARE signaling in response to oxidative stress [26]. Interestingly, taxa in genus Lactobacillus have been identified in mosquito microbiota [7, 27].…”

Section: Nrf2 Signaling In Oxidative Stress Responsementioning

confidence: 99%

The impact of metagenomic interplay on the mosquito redox homeostasis

Champion

2017

Free Radical Biology and Medicine

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Mosquitoes are exposed to oxidative challenges throughout their life cycle. The primary challenge comes from a blood meal. The blood digestion turns the midgut into an oxidative environment, which imposes pressure not only on mosquito fecundity and other physiological traits but also on the microbiota in the midgut. During evolution, mosquitoes have developed numerous oxidative defense mechanisms to maintain redox homeostasis in the midgut. In addition to antioxidants, SOD, catalase, and glutathione system, sufficient supply of the reducing agent, NADPH, is vital for a successful defense against oxidative stress. Increasing evidence indicates that in response to oxidative stress, cells reconfigure metabolic pathways to increase the generation of NADPH through NADP-reducing networks including the pentose phosphate pathway and others. The microbial homeostasis is critical for the functional contributions to various host phenotypes. The symbiotic microbiota is regulated largely by the Duox-ROS pathway in Drosophila. In mosquitoes, Duox-ROS pathway, heme-mediated signaling, antimicrobial peptide production and C-type lectins work in concert to maintain the dynamic microbial community in the midgut. Microbial mechanisms against oxidative stress in this context are not well understood. Emerging evidence that microbial metabolites trigger host oxidative response warrants further study on the metagenomic interplay in an oxidative environment like mosquito gut ecosystem. Besides the classical Drosophila model, hematophagous insects like mosquitoes provide an alternative model system to study redox homeostasis in a symbiotic metagenomic context.

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10-Oxo-trans-11-octadecenoic acid generated from linoleic acid by a gut lactic acid bacterium Lactobacillus plantarum is cytoprotective against oxidative stress

Cited by 48 publications

References 49 publications

High Fat Diet-Induced Hepatic 18-Carbon Fatty Acids Accumulation Up-Regulates CYP2A5/CYP2A6 via NF-E2-Related Factor 2

High Fat Diet-Induced Hepatic 18-Carbon Fatty Acids Accumulation Up-Regulates CYP2A5/CYP2A6 via NF-E2-Related Factor 2

Environmental Factors, Gut Microbiota, and Colorectal Cancer Prevention

The impact of metagenomic interplay on the mosquito redox homeostasis

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