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Journal articles on the topic 'Gut toxicity'

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Author: Grafiati
Published: 10 December 2022
Last updated: 28 January 2023

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1

SMITH, C. "NSAIDs and gut toxicity." Lancet 344, no. 8914 (July 1994): 56–57. http://dx.doi.org/10.1016/s0140-6736(94)91077-4.

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2

Leddin, Desmond J., and Kevork M. Peltekian. "Gut Toxicity of 5-ASA?" Canadian Journal of Gastroenterology 7, no. 2 (1993): 170–72. http://dx.doi.org/10.1155/1993/781293.

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3

Tu, Pengcheng, Liang Chi, Wanda Bodnar, Zhenfa Zhang, Bei Gao, Xiaoming Bian, Jill Stewart, Rebecca Fry, and Kun Lu. "Gut Microbiome Toxicity: Connecting the Environment and Gut Microbiome-Associated Diseases." Toxics 8, no. 1 (March 12, 2020): 19. http://dx.doi.org/10.3390/toxics8010019.

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The human gut microbiome can be easily disturbed upon exposure to a range of toxic environmental agents. Environmentally induced perturbation in the gut microbiome is strongly associated with human disease risk. Functional gut microbiome alterations that may adversely influence human health is an increasingly appreciated mechanism by which environmental chemicals exert their toxic effects. In this review, we define the functional damage driven by environmental exposure in the gut microbiome as gut microbiome toxicity. The establishment of gut microbiome toxicity links the toxic effects of various environmental agents and microbiota-associated diseases, calling for more comprehensive toxicity evaluation with extended consideration of gut microbiome toxicity.
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4

Bateman, D. N. "NSAIDs: time to re-evaluate gut toxicity." Lancet 343, no. 8905 (April 1994): 1051–52. http://dx.doi.org/10.1016/s0140-6736(94)90175-9.

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5

Tinkov, Alexey A., Viktor A. Gritsenko, Margarita G. Skalnaya, Sergey V. Cherkasov, Jan Aaseth, and Anatoly V. Skalny. "Gut as a target for cadmium toxicity." Environmental Pollution 235 (April 2018): 429–34. http://dx.doi.org/10.1016/j.envpol.2017.12.114.

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6

Kaliannan, Kanakaraju, Shane O. Donnell, Kiera Murphy, Catherine Stanton, Chao Kang, Bin Wang, Xiang-Yong Li, Atul K. Bhan, and Jing X. Kang. "Decreased Tissue Omega-6/Omega-3 Fatty Acid Ratio Prevents Chemotherapy-Induced Gastrointestinal Toxicity Associated with Alterations of Gut Microbiome." International Journal of Molecular Sciences 23, no. 10 (May 10, 2022): 5332. http://dx.doi.org/10.3390/ijms23105332.

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Gastrointestinal toxicity (GIT) is a debilitating side effect of Irinotecan (CPT-11) and limits its clinical utility. Gut dysbiosis has been shown to mediate this side effect of CPT-11 by increasing gut bacterial β-glucuronidase (GUSB) activity and impairing the intestinal mucosal barrier (IMB). We have recently shown the opposing effects of omega-6 (n-6) and omega-3 (n-3) polyunsaturated fatty acids (PUFA) on the gut microbiome. We hypothesized that elevated levels of tissue n-3 PUFA with a decreased n-6/n-3 PUFA ratio would reduce CPT-11-induced GIT and associated changes in the gut microbiome. Using a unique transgenic mouse (FAT-1) model combined with dietary supplementation experiments, we demonstrate that an elevated tissue n-3 PUFA status with a decreased n-6/n-3 PUFA ratio significantly reduces CPT-11-induced weight loss, bloody diarrhea, gut pathological changes, and mortality. Gut microbiome analysis by 16S rRNA gene sequencing and QIIME2 revealed that improvements in GIT were associated with the reduction in the CPT-11-induced increase in both GUSB-producing bacteria (e.g., Enterobacteriaceae) and GUSB enzyme activity, decrease in IMB-maintaining bacteria (e.g., Bifidobacterium), IMB dysfunction and systemic endotoxemia. These results uncover a host–microbiome interaction approach to the management of drug-induced gut toxicity. The prevention of CPT-11-induced gut microbiome changes by decreasing the tissue n-6/n-3 PUFA ratio could be a novel strategy to prevent chemotherapy-induced GIT.
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7

Feng, Pengya, Ze Ye, Apurva Kakade, Amanpreet Virk, Xiangkai Li, and Pu Liu. "A Review on Gut Remediation of Selected Environmental Contaminants: Possible Roles of Probiotics and Gut Microbiota." Nutrients 11, no. 1 (December 21, 2018): 22. http://dx.doi.org/10.3390/nu11010022.

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Various environmental contaminants including heavy metals, pesticides and antibiotics can contaminate food and water, leading to adverse effects on human health, such as inflammation, oxidative stress and intestinal disorder. Therefore, remediation of the toxicity of foodborne contaminants in human has become a primary concern. Some probiotic bacteria, mainly Lactobacilli, have received a great attention due to their ability to reduce the toxicity of several contaminants. For instance, Lactobacilli can reduce the accumulation and toxicity of selective heavy metals and pesticides in animal tissues by inhibiting intestinal absorption of contaminants and enhancing intestinal barrier function. Probiotics have also shown to decrease the risk of antibiotic-associated diarrhea possibly via competing and producing antagonistic compounds against pathogenic bacteria. Furthermore, probiotics can improve immune function by enhancing the gut microbiota mediated anti-inflammation. Thus, these probiotic bacteria are promising candidates for protecting body against foodborne contaminants-induced toxicity. Study on the mechanism of these beneficial bacterial strains during remediation processes and particularly their interaction with host gut microbiota is an active field of research. This review summarizes the current understanding of the remediation mechanisms of some probiotics and the combined effects of probiotics and gut microbiota on remediation of foodborne contaminants in vivo.
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8

Coryell, Michael, Barbara A. Roggenbeck, and Seth T. Walk. "The Human Gut Microbiome’s Influence on Arsenic Toxicity." Current Pharmacology Reports 5, no. 6 (November 25, 2019): 491–504. http://dx.doi.org/10.1007/s40495-019-00206-4.

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Abstract Purpose of Review Arsenic exposure is a public health concern of global proportions with a high degree of interindividual variability in pathologic outcomes. Arsenic metabolism is a key factor underlying toxicity, and the primary purpose of this review is to summarize recent discoveries concerning the influence of the human gut microbiome on the metabolism, bioavailability, and toxicity of ingested arsenic. We review and discuss the current state of knowledge along with relevant methodologies for studying these phenomena. Recent Findings Bacteria in the human gut can biochemically transform arsenic-containing compounds (arsenicals). Recent publications utilizing culture-based approaches combined with analytical biochemistry and molecular genetics have helped identify several arsenical transformations by bacteria that are at least possible in the human gut and are likely to mediate arsenic toxicity to the host. Other studies that directly incubate stool samples in vitro also demonstrate the gut microbiome’s potential to alter arsenic speciation and bioavailability. In vivo disruption or elimination of the microbiome has been shown to influence toxicity and body burden of arsenic through altered excretion and biotransformation of arsenicals. Currently, few clinical or epidemiological studies have investigated relationships between the gut microbiome and arsenic-related health outcomes in humans, although current evidence provides strong rationale for this research in the future. Summary The human gut microbiome can metabolize arsenic and influence arsenical oxidation state, methylation status, thiolation status, bioavailability, and excretion. We discuss the strength of current evidence and propose that the microbiome be considered in future epidemiologic and toxicologic studies of human arsenic exposure.
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9

Alexander, James L., Ian D. Wilson, Julian Teare, Julian R. Marchesi, Jeremy K. Nicholson, and James M. Kinross. "Gut microbiota modulation of chemotherapy efficacy and toxicity." Nature Reviews Gastroenterology & Hepatology 14, no. 6 (March 8, 2017): 356–65. http://dx.doi.org/10.1038/nrgastro.2017.20.

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10

ZUBERI, B. F. "Lidocaine toxicity in a student undergoing upper gastrointestinal endoscopy." Gut 46, no. 3 (March 1, 2000): 435. http://dx.doi.org/10.1136/gut.46.3.435.

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11

Sturgess, R. P., H. J. Ellis, and P. J. Ciclitira. "Cereal chemistry, molecular biology, and toxicity in coeliac disease." Gut 32, no. 9 (September 1, 1991): 1055–60. http://dx.doi.org/10.1136/gut.32.9.1055.

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12

Chen, Zhangjian, Shuo Han, Di Zhou, Shupei Zhou, and Guang Jia. "Effects of oral exposure to titanium dioxide nanoparticles on gut microbiota and gut-associated metabolism in vivo." Nanoscale 11, no. 46 (2019): 22398–412. http://dx.doi.org/10.1039/c9nr07580a.

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13

Fraser, J. S. "Coeliac disease: in vivo toxicity of the putative immunodominant epitope." Gut 52, no. 12 (December 1, 2003): 1698–702. http://dx.doi.org/10.1136/gut.52.12.1698.

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14

Flack, Amanda, Amanda L. Persons, Sharanya M. Kousik, T. Celeste Napier, and Anna Moszczynska. "Self-administration of methamphetamine alters gut biomarkers of toxicity." European Journal of Neuroscience 46, no. 3 (August 2017): 1918–32. http://dx.doi.org/10.1111/ejn.13630.

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15

Allison, Susan J. "Gut microbes: a role in melamine-induced renal toxicity?" Nature Reviews Nephrology 9, no. 4 (March 5, 2013): 186. http://dx.doi.org/10.1038/nrneph.2013.28.

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16

Al-Dasooqi, Noor. "Matrix metalloproteinases and gut toxicity following cytotoxic cancer therapy." Current Opinion in Supportive and Palliative Care 8, no. 2 (June 2014): 164–69. http://dx.doi.org/10.1097/spc.0000000000000049.

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17

Wilson, Ian D., and Jeremy K. Nicholson. "Gut microbiome interactions with drug metabolism, efficacy, and toxicity." Translational Research 179 (January 2017): 204–22. http://dx.doi.org/10.1016/j.trsl.2016.08.002.

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18

Ninkov, Marina, Aleksandra Popov Aleksandrov, Jelena Demenesku, Ivana Mirkov, Dina Mileusnic, Anja Petrovic, Ilijana Grigorov, et al. "Toxicity of oral cadmium intake: Impact on gut immunity." Toxicology Letters 237, no. 2 (September 2015): 89–99. http://dx.doi.org/10.1016/j.toxlet.2015.06.002.

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19

Gibson, Rachel J., Janet K. Coller, Hannah R. Wardill, Mark R. Hutchinson, Scott Smid, and Joanne M. Bowen. "Chemotherapy-induced gut toxicity and pain: involvement of TLRs." Supportive Care in Cancer 24, no. 5 (November 19, 2015): 2251–58. http://dx.doi.org/10.1007/s00520-015-3020-2.

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20

Fuller, Roy. "Role of the gut flora in toxicity and cancer." Food and Chemical Toxicology 27, no. 1 (January 1989): 66. http://dx.doi.org/10.1016/0278-6915(89)90096-3.

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21

Dubrow, Robert. "Role of the gut flora in toxicity and cancer." Gastroenterology 96, no. 4 (April 1989): 1221. http://dx.doi.org/10.1016/0016-5085(89)91650-8.

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22

Drobne, Damjana, Maja Rupnik, Ales Lapanje, Jasna Strus, and Miha Janc. "Isopod gut microflora parameters as endpoints in toxicity studies." Environmental Toxicology and Chemistry 21, no. 3 (March 2002): 604–9. http://dx.doi.org/10.1002/etc.5620210320.

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23

Gori, Stefania, Alessandro Inno, Lorenzo Belluomini, Paolo Bocus, Zeno Bisoffi, Antonio Russo, and Guido Arcaro. "Gut microbiota and cancer: How gut microbiota modulates activity, efficacy and toxicity of antitumoral therapy." Critical Reviews in Oncology/Hematology 143 (November 2019): 139–47. http://dx.doi.org/10.1016/j.critrevonc.2019.09.003.

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24

Cuffari, C., Y. Theoret, S. Latour, and G. Seidman. "6-Mercaptopurine metabolism in Crohn's disease: correlation with efficacy and toxicity." Gut 39, no. 3 (September 1, 1996): 401–6. http://dx.doi.org/10.1136/gut.39.3.401.

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25

Liu, Yang, Siyuan Xu, Qiudie Cai, Dawei Li, Hongye Li, and Weidong Yang. "In Vitro Interactions between Okadaic Acid and Rat Gut Microbiome." Marine Drugs 20, no. 9 (August 30, 2022): 556. http://dx.doi.org/10.3390/md20090556.

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Okadaic acid (OA) is a marine biotoxin associated with diarrhetic shellfish poisoning (DSP), posing some threat to human beings. The oral toxicity of OA is complex, and the mechanism of toxicity is not clear. The interaction between OA and gut microbiota may provide a reasonable explanation for the complex toxicity of OA. Due to the complex environment in vivo, an in vitro study may be better for the interactions between OA and gut microbiome. Here, we conducted an in vitro fermentation experiment of gut bacteria in the presence of 0–1000 nM OA. The remolding ability of OA on bacterial composition was investigated by 16S rDNA sequencing, and differential metabolites in fermentation system with different concentration of OA was detected by LC-MS/MS. We found that OA inhibited some specific bacterial genera but promoted others. In addition, eight possible metabolites of OA, including dinophysistoxin-2 (DTX-2), were detected in the fermentation system. The abundance of Faecalitalea was strongly correlated with the possible metabolites of OA, suggesting that Faecalitalea may be involved in the metabolism of OA in vitro. Our findings confirmed the direct interaction between OA and gut bacteria, which helps to reveal the metabolic process of OA and provide valuable evidence for elucidating the complex toxicity of OA.
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26

Zeng, Xiaozhou, Zhihong Liu, Yanxi Dong, Jiamin Zhao, Bin Wang, Huiwen Xiao, Yuan Li, et al. "Social Hierarchy Dictates Intestinal Radiation Injury in a Gut Microbiota-Dependent Manner." International Journal of Molecular Sciences 23, no. 21 (October 29, 2022): 13189. http://dx.doi.org/10.3390/ijms232113189.

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Social hierarchy governs the physiological and biochemical behaviors of animals. Intestinal radiation injuries are common complications connected with radiotherapy. However, it remains unclear whether social hierarchy impacts the development of radiation-induced intestinal toxicity. Dominant mice exhibited more serious intestinal toxicity following total abdominal irradiation compared with their subordinate counterparts, as judged by higher inflammatory status and lower epithelial integrity. Radiation-elicited changes in gut microbiota varied between dominant and subordinate mice, being more overt in mice of higher status. Deletion of gut microbes by using an antibiotic cocktail or restructuring of the gut microecology of dominant mice by using fecal microbiome from their subordinate companions erased the difference in radiogenic intestinal injuries. Lactobacillus murinus and Akkermansia muciniphila were both found to be potential probiotics for use against radiation toxicity in mouse models without social hierarchy. However, only Akkermansia muciniphila showed stable colonization in the digestive tracts of dominant mice, and significantly mitigated their intestinal radiation injuries. Our findings demonstrate that social hierarchy impacts the development of radiation-induced intestinal injuries, in a manner dependent on gut microbiota. The results also suggest that the gut microhabitats of hosts determine the colonization and efficacy of foreign probiotics. Thus, screening suitable microbial preparations based on the gut microecology of patients might be necessary in clinical application.
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27

Chen, Jianjun, Dandan Sun, Han Cui, Chenyang Rao, Lulu Li, Suqi Guo, Shuai Yang, Yuru Zhang, and Xianglin Cao. "Toxic effects of carbon quantum dots on the gut–liver axis and gut microbiota in the common carp Cyprinus carpio." Environmental Science: Nano 9, no. 1 (2022): 173–88. http://dx.doi.org/10.1039/d1en00651g.

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28

Pontoppidan, Peter EL, René L. Shen, Malene S. Cilieborg, Pingping Jiang, Hannelouise Kissow, Bodil L. Petersen, Thomas Thymann, Carsten Heilmann, Klaus Müller, and Per T. Sangild. "Bovine Colostrum Modulates Myeloablative Chemotherapy–Induced Gut Toxicity in Piglets." Journal of Nutrition 145, no. 7 (May 27, 2015): 1472–80. http://dx.doi.org/10.3945/jn.114.203430.

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29

Zheng, X., A. Zhao, G. Xie, Y. Chi, L. Zhao, H. Li, C. Wang, et al. "Melamine-Induced Renal Toxicity Is Mediated by the Gut Microbiota." Science Translational Medicine 5, no. 172 (February 13, 2013): 172ra22. http://dx.doi.org/10.1126/scitranslmed.3005114.

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30

Goebel, Carsten, Katja Kirchhoff, Hermann Wasmuth, Stefanie Flohé, Robert B. Elliott, and Hubert Kolb. "The gut cytokine balance as a target of lead toxicity." Life Sciences 64, no. 24 (May 1999): 2207–14. http://dx.doi.org/10.1016/s0024-3205(99)00172-1.

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31

Li, Houkai, Jiaojiao He, and Wei Jia. "The influence of gut microbiota on drug metabolism and toxicity." Expert Opinion on Drug Metabolism & Toxicology 12, no. 1 (December 10, 2015): 31–40. http://dx.doi.org/10.1517/17425255.2016.1121234.

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32

Swann, Jonathan, Yulan Wang, Leticia Abecia, Adele Costabile, Kieran Tuohy, Glenn Gibson, David Roberts, et al. "Gut microbiome modulates the toxicity of hydrazine: a metabonomic study." Molecular BioSystems 5, no. 4 (2009): 351. http://dx.doi.org/10.1039/b811468d.

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33

Guerre, Philippe. "Mycotoxin and Gut Microbiota Interactions." Toxins 12, no. 12 (December 4, 2020): 769. http://dx.doi.org/10.3390/toxins12120769.

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The interactions between mycotoxins and gut microbiota were discovered early in animals and explained part of the differences in susceptibility to mycotoxins among species. Isolation of microbes present in the gut responsible for biotransformation of mycotoxins into less toxic metabolites and for binding mycotoxins led to the development of probiotics, enzymes, and cell extracts that are used to prevent mycotoxin toxicity in animals. More recently, bioactivation of mycotoxins into toxic compounds, notably through the hydrolysis of masked mycotoxins, revealed that the health benefits of the effect of the gut microbiota on mycotoxins can vary strongly depending on the mycotoxin and the microbe concerned. Interactions between mycotoxins and gut microbiota can also be observed through the effect of mycotoxins on the gut microbiota. Changes of gut microbiota secondary to mycotoxin exposure may be the consequence of the antimicrobial properties of mycotoxins or the toxic effect of mycotoxins on epithelial and immune cells in the gut, and liberation of antimicrobial peptides by these cells. Whatever the mechanism involved, exposure to mycotoxins leads to changes in the gut microbiota composition at the phylum, genus, and species level. These changes can lead to disruption of the gut barrier function and bacterial translocation. Changes in the gut microbiota composition can also modulate the toxicity of toxic compounds, such as bacterial toxins and of mycotoxins themselves. A last consequence for health of the change in the gut microbiota secondary to exposure to mycotoxins is suspected through variations observed in the amount and composition of the volatile fatty acids and sphingolipids that are normally present in the digesta, and that can contribute to the occurrence of chronic diseases in human. The purpose of this work is to review what is known about mycotoxin and gut microbiota interactions, the mechanisms involved in these interactions, and their practical application, and to identify knowledge gaps and future research needs.
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34

Dieterich, W. "Cross linking to tissue transglutaminase and collagen favours gliadin toxicity in coeliac disease." Gut 55, no. 4 (April 1, 2006): 478–84. http://dx.doi.org/10.1136/gut.2005.069385.

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35

Alkharabsheh, Omar, M. Hasib Sidiqi, Mohammed A. Aljama, Morie A. Gertz, and Arthur E. Frankel. "The Human Microbiota in Multiple Myeloma and Proteasome Inhibitors." Acta Haematologica 143, no. 2 (July 16, 2019): 118–23. http://dx.doi.org/10.1159/000500976.

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The gut microbiota plays a significant role in health and disease, including cancer development and treatment. The importance of the gut microbiota in the efficacy and toxicity of novel therapies and immunotherapy is increasingly recognized. Plasma cells in multiple myeloma have the potential to survive in the gastrointestinal tract for long periods of time. The nature of the gut microbiota impacts the degree of antigen stimulation of these cells and may play a role in mutation development and clonal evolution. Furthermore, myeloma therapies such as proteasome inhibitors and alkylating agents, commonly used to treat patients, are frequently associated with gastrointestinal adverse events. Herein we review the gut microbiota and its role in hematopoiesis, pathogenesis of myeloma, and efficacy/toxicity of anti-myeloma therapies.
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36

Sutherland, Vicki L., Charlene A. McQueen, Donna Mendrick, Donna Gulezian, Carl Cerniglia, Steven Foley, Sam Forry, et al. "The Gut Microbiome and Xenobiotics: Identifying Knowledge Gaps." Toxicological Sciences 176, no. 1 (June 25, 2020): 1–10. http://dx.doi.org/10.1093/toxsci/kfaa060.

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Abstract There is an increasing awareness that the gut microbiome plays a critical role in human health and disease, but mechanistic insights are often lacking. In June 2018, the Health and Environmental Sciences Institute (HESI) held a workshop, “The Gut Microbiome: Markers of Human Health, Drug Efficacy and Xenobiotic Toxicity” (https://hesiglobal.org/event/the-gut-microbiome-workshop) to identify data gaps in determining how gut microbiome alterations may affect human health. Speakers and stakeholders from academia, government, and industry addressed multiple topics including the current science on the gut microbiome, endogenous and exogenous metabolites, biomarkers, and model systems. The workshop presentations and breakout group discussions formed the basis for identifying data gaps and research needs. Two critical issues that emerged were defining the microbial composition and function related to health and developing standards for models, methods and analysis in order to increase the ability to compare and replicate studies. A series of key recommendations were formulated to focus efforts to further understand host-microbiome interactions and the consequences of exposure to xenobiotics as well as identifying biomarkers of microbiome-associated disease and toxicity.
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37

Yuan, Ge-hui, Zhan Zhang, Xing-su Gao, Jun Zhu, Wen-hui Guo, Li Wang, Ping Ding, Ping Jiang, and Lei Li. "Gut microbiota-mediated tributyltin-induced metabolic disorder in rats." RSC Advances 10, no. 71 (2020): 43619–28. http://dx.doi.org/10.1039/d0ra07502g.

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Tributyltin (TBT), an environmental pollutant widely used in antifouling coatings, can cause multiple-organ toxicity and gut microbiome dysbiosis in organisms, and can even cause changes in the host metabolomic profiles.
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38

Connell, W. R., M. A. Kamm, J. K. Ritchie, and J. E. Lennard-Jones. "Bone marrow toxicity caused by azathioprine in inflammatory bowel disease: 27 years of experience." Gut 34, no. 8 (August 1, 1993): 1081–85. http://dx.doi.org/10.1136/gut.34.8.1081.

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39

Bacchetta, Renato, Anna Winkler, Nadia Santo, and Paolo Tremolada. "The Toxicity of Polyester Fibers in Xenopuslaevis." Water 13, no. 23 (December 4, 2021): 3446. http://dx.doi.org/10.3390/w13233446.

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Microplastics are practically ubiquitous and pose a serious survival challenge for many species. Most of the exposure experiments for determining the toxicological effects of microplastics were performed with a microplastic varying little in shape and size (often purchased microplastic beads), but few studies deal with non-homogeneous samples. We analyzed the effect on Xenopuslaevis larva on the early development of polyester fibers, PEFs, taken from a dryer machine in which 100% polyester fabrics were dried after washing. Three concentrations were tested. The results showed that the gastrointestinal tract, GIT, was the most affected system by PEFs which modified the normal shape of the intestine with an EC50 96 h value of 6.3 µg mL−1. Fibers were observed to press against the digestive epithelium, deforming the normal architecture of the gut, sometimes pushing deep into the epithelium until piercing it. Physical GIT occlusion was observed in a concentration-dependent manner. However, no other damages were registered. No mortality was observed, but PEF-exposed larvae showed a significant reduction in their mobility. The results of the present paper suggest that environmental samples with their heterogeneity may have adverse effects on X. laevis development.
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40

Huang, Xiaoquan, and Meng Tang. "Review of gut nanotoxicology in mammals: Exposure, transformation, distribution and toxicity." Science of The Total Environment 773 (June 2021): 145078. http://dx.doi.org/10.1016/j.scitotenv.2021.145078.

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41

Leveque, M., C. Stoffels, E. Person, I. Fourquaux, V. Theodorou, H. Robert, N. Cabaton, J. N. Audinot, and M. Mercier-Bonin. "Uptake, fate, and gut toxicity of perfluorooctanoic acid (PFOA) in vitro." Toxicology Letters 350 (September 2021): S231. http://dx.doi.org/10.1016/s0378-4274(21)00778-5.

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42

Liu, Jing-Bo, Kai Chen, Zi-Fa Li, Zhen-Yong Wang, and Lin Wang. "Glyphosate-induced gut microbiota dysbiosis facilitates male reproductive toxicity in rats." Science of The Total Environment 805 (January 2022): 150368. http://dx.doi.org/10.1016/j.scitotenv.2021.150368.

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43

Huang, Xinyi, Lulu Chen, Zhenyu Li, Binjie Zheng, Na Liu, Qing Fang, Jinsheng Jiang, Tai Rao, and Dongsheng Ouyang. "The efficacy and toxicity of antineoplastic antimetabolites: Role of gut microbiota." Toxicology 460 (August 2021): 152858. http://dx.doi.org/10.1016/j.tox.2021.152858.

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44

Yu-ting, Wang. "Fate and Toxicity of Organic Pollutants in Earthworm Gut: A Review." IOP Conference Series: Earth and Environmental Science 199 (December 19, 2018): 022055. http://dx.doi.org/10.1088/1755-1315/199/2/022055.

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45

Shen, René L., Mathias Rathe, Pingping Jiang, Peter E. L. Pontoppidan, Peter M. H. Heegaard, Klaus Müller, and Per T. Sangild. "Doxorubicin-Induced Gut Toxicity in Piglets Fed Bovine Milk and Colostrum." Journal of Pediatric Gastroenterology and Nutrition 63, no. 6 (December 2016): 698–707. http://dx.doi.org/10.1097/mpg.0000000000001205.

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46

Ervin, Samantha M., Ronan P. Hanley, Lauren Lim, William G. Walton, Kenneth H. Pearce, Aadra P. Bhatt, Lindsey I. James, and Matthew R. Redinbo. "Targeting Regorafenib-Induced Toxicity through Inhibition of Gut Microbial β-Glucuronidases." ACS Chemical Biology 14, no. 12 (October 30, 2019): 2737–44. http://dx.doi.org/10.1021/acschembio.9b00663.

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47

Yuan, Xianling, Zihong Pan, Cuiyuan Jin, Yinhua Ni, Zhengwei Fu, and Yuanxiang Jin. "Gut microbiota: An underestimated and unintended recipient for pesticide-induced toxicity." Chemosphere 227 (July 2019): 425–34. http://dx.doi.org/10.1016/j.chemosphere.2019.04.088.

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48

Wardill, Hannah R., Joanne M. Bowen, and Rachel J. Gibson. "Chemotherapy-induced gut toxicity: are alterations to intestinal tight junctions pivotal?" Cancer Chemotherapy and Pharmacology 70, no. 5 (September 30, 2012): 627–35. http://dx.doi.org/10.1007/s00280-012-1989-5.

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49

Ma, Li, Mingzheng Duan, Ziwei He, Yu Zhang, Yiting Chen, Bo Li, Muhammad Junaid Rao, Lihua Hu, and Lingqiang Wang. "Sugarcane Wax Metabolites and Their Toxicity to Silkworms." Life 13, no. 2 (January 19, 2023): 286. http://dx.doi.org/10.3390/life13020286.

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Abstract:
Sugarcane wax has the potential to be utilized as a novel natural insecticide, which could help to reduce the large yield losses caused by agricultural pests. By employing the gas chromatography–mass spectrometry (GC-MS) approach, we conducted a study to analyze the composition of epicuticular wax from the rind of the sugarcane variety YT71210. A total of 157 metabolites, categorized into 15 classes, were identified, with naphthalene, a metabolite with insect-resistant properties, being the most prevalent. The feeding trial experiment suggested that sugarcane wax is toxic to silkworms by impacting the internal organs. Intestinal microbial diversity analysis suggested that the abundance of Enterococcus genus was significantly increased in both ordure and gut of silkworm after wax treatment. The results indicated that the feeding of wax has an adverse effect on the gut microbial composition of silkworms. Our findings lay a foundation for the efficacy of sugarcane waxes as a valuable natural insecticide and for the prediction of promising sugarcane varieties with insect resistance.
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Runzi, M., B. M. Peskar, J. von Schonfeld, and M. K. Muller. "Importance of endogenous prostaglandins for the toxicity of cyclosporin A to rat endocrine and exocrine pancreas?" Gut 33, no. 11 (November 1, 1992): 1572–77. http://dx.doi.org/10.1136/gut.33.11.1572.

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