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Authors = Bill J. Gurley

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14 pages, 12612 KiB  
Article
Safety and Molecular-Toxicological Implications of Cannabidiol-Rich Cannabis Extract and Methylsulfonylmethane Co-Administration
by Kristy R. Kutanzi, Laura E. Ewing, Charles M. Skinner, Charles M. Quick, Stefanie Kennon-McGill, Mitchell R. McGill, Larry A. Walker, Mahmoud A. ElSohly, Bill J. Gurley and Igor Koturbash
Int. J. Mol. Sci. 2020, 21(20), 7808; https://doi.org/10.3390/ijms21207808 - 21 Oct 2020
Cited by 8 | Viewed by 5725
Abstract
Cannabidiol (CBD) is a biologically active, non-psychotropic component of Cannabis sativa whose popularity has grown exponentially in recent years. Besides a wealth of potential health benefits, ingestion of CBD poses risks for a number of side effects, of which hepatotoxicity and CBD/herb-drug interactions [...] Read more.
Cannabidiol (CBD) is a biologically active, non-psychotropic component of Cannabis sativa whose popularity has grown exponentially in recent years. Besides a wealth of potential health benefits, ingestion of CBD poses risks for a number of side effects, of which hepatotoxicity and CBD/herb-drug interactions are of particular concern. Here, we investigated the interaction potential between the cannabidiol-rich cannabis extract (CRCE) and methylsulfonylmethane (MSM), a popular dietary supplement, in the mouse model. For this purpose, 8-week-old male C57BL6/J mice received MSM-containing water (80 mg/100 mL) ad libitum for 17 days. During the last three days of treatment, mice received three doses of CRCE administered in sesame oil via oral gavage (123 mg/kg/day). Administration of MSM alone did not result in any evidence of liver toxicity and did not induce expression of mouse cytochrome P450 (CYP) enzymes. Administration of CRCE did produce significant (p < 0.05) increases in Cyp1a2, Cyp2b10, Cyp2c29, Cyp3a4, Cyp3a11, Cyp2c65, and Cyp2c66 messenger RNA, however, this effect was not amplified by MSM/CRCE co-treatment. Similarly, no evidence of liver toxicity was observed in MSM/CRCE dosed mice. In conclusion, short-term MSM/CRCE co-administration did not demonstrate any evidence of hepatotoxicity in the mouse model. Full article
(This article belongs to the Special Issue Innovative Molecular Methodologies and Models in Assessing the Toxicity Potential of Natural Products)
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12 pages, 2607 KiB  
Article
Paradoxical Patterns of Sinusoidal Obstruction Syndrome-Like Liver Injury in Aged Female CD-1 Mice Triggered by Cannabidiol-Rich Cannabis Extract and Acetaminophen Co-Administration
by Laura E. Ewing, Mitchell R. McGill, Eric U. Yee, Charles M. Quick, Charles M. Skinner, Stefanie Kennon-McGill, Melissa Clemens, Joel H. Vazquez, Sandra S. McCullough, D. Keith Williams, Kristy R. Kutanzi, Larry A. Walker, Mahmoud A. ElSohly, Laura P. James, Bill J. Gurley and Igor Koturbash
Molecules 2019, 24(12), 2256; https://doi.org/10.3390/molecules24122256 - 17 Jun 2019
Cited by 28 | Viewed by 9403
Abstract
The goal of this study was to investigate the potential for a cannabidiol-rich cannabis extract (CRCE) to interact with the most common over-the-counter drug and the major known cause of drug-induced liver injury–acetaminophen (APAP)–in aged female CD-1 mice. Gavaging mice with 116 mg/kg [...] Read more.
The goal of this study was to investigate the potential for a cannabidiol-rich cannabis extract (CRCE) to interact with the most common over-the-counter drug and the major known cause of drug-induced liver injury–acetaminophen (APAP)–in aged female CD-1 mice. Gavaging mice with 116 mg/kg of cannabidiol (CBD) [mouse equivalent dose (MED) of 10 mg/kg of CBD] in CRCE delivered with sesame oil for three consecutive days followed by intraperitoneally (i.p.) acetaminophen (APAP) administration (400 mg/kg) on day 4 resulted in overt toxicity with 37.5% mortality. No mortality was observed in mice treated with 290 mg/kg of CBD+APAP (MED of 25 mg/kg of CBD) or APAP alone. Following CRCE/APAP co-administration, microscopic examination revealed a sinusoidal obstruction syndrome-like liver injury–the severity of which correlated with the degree of alterations in physiological and clinical biochemistry end points. Mechanistically, glutathione depletion and oxidative stress were observed between the APAP-only and co-administration groups, but co-administration resulted in much greater activation of c-Jun N-terminal kinase (JNK). Strikingly, these effects were not observed in mice gavaged with 290 mg/kg CBD in CRCE followed by APAP administration. These findings highlight the potential for CBD/drug interactions, and reveal an interesting paradoxical effect of CBD/APAP-induced hepatotoxicity. Full article
(This article belongs to the Special Issue Cytotoxic Activity of Plant Extracts)
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17 pages, 5638 KiB  
Article
Hepatotoxicity of a Cannabidiol-Rich Cannabis Extract in the Mouse Model
by Laura E. Ewing, Charles M. Skinner, Charles M. Quick, Stefanie Kennon-McGill, Mitchell R. McGill, Larry A. Walker, Mahmoud A. ElSohly, Bill J. Gurley and Igor Koturbash
Molecules 2019, 24(9), 1694; https://doi.org/10.3390/molecules24091694 - 30 Apr 2019
Cited by 122 | Viewed by 143905
Abstract
The goal of this study was to investigate Cannabidiol (CBD) hepatotoxicity in 8-week-old male B6C3F1 mice. Animals were gavaged with either 0, 246, 738, or 2460 mg/kg of CBD (acute toxicity, 24 h) or with daily doses of 0, 61.5, 184.5, or [...] Read more.
The goal of this study was to investigate Cannabidiol (CBD) hepatotoxicity in 8-week-old male B6C3F1 mice. Animals were gavaged with either 0, 246, 738, or 2460 mg/kg of CBD (acute toxicity, 24 h) or with daily doses of 0, 61.5, 184.5, or 615 mg/kg for 10 days (sub-acute toxicity). These doses were the allometrically scaled mouse equivalent doses (MED) of the maximum recommended human maintenance dose of CBD in EPIDIOLEX® (20 mg/kg). In the acute study, significant increases in liver-to-body weight (LBW) ratios, plasma ALT, AST, and total bilirubin were observed for the 2460 mg/kg dose. In the sub-acute study, 75% of mice gavaged with 615 mg/kg developed a moribund condition between days three and four. As in the acute phase, 615 mg/kg CBD increased LBW ratios, ALT, AST, and total bilirubin. Hepatotoxicity gene expression arrays revealed that CBD differentially regulated more than 50 genes, many of which were linked to oxidative stress responses, lipid metabolism pathways and drug metabolizing enzymes. In conclusion, CBD exhibited clear signs of hepatotoxicity, possibly of a cholestatic nature. The involvement of numerous pathways associated with lipid and xenobiotic metabolism raises serious concerns about potential drug interactions as well as the safety of CBD. Full article
(This article belongs to the Special Issue Plant Extracts: Biological and Pharmacological Activity)
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14 pages, 1318 KiB  
Article
Decaffeinated Green Tea Extract Does Not Elicit Hepatotoxic Effects and Modulates the Gut Microbiome in Lean B6C3F1 Mice
by Bill J. Gurley, Isabelle R. Miousse, Intawat Nookaew, Laura E. Ewing, Charles M. Skinner, Piroon Jenjaroenpun, Thidathip Wongsurawat, Stefanie Kennon-McGill, Bharathi Avula, Ji-Yeong Bae, Mitchell R. McGill, David Ussery, Ikhlas A. Khan and Igor Koturbash
Nutrients 2019, 11(4), 776; https://doi.org/10.3390/nu11040776 - 3 Apr 2019
Cited by 19 | Viewed by 6070
Abstract
The main purpose of this study was to investigate the hepatotoxic potential and effects on the gut microbiome of decaffeinated green tea extract (dGTE) in lean B6C3F1 mice. Gavaging dGTE over a range of 1X–10X mouse equivalent doses (MED) for up to [...] Read more.
The main purpose of this study was to investigate the hepatotoxic potential and effects on the gut microbiome of decaffeinated green tea extract (dGTE) in lean B6C3F1 mice. Gavaging dGTE over a range of 1X–10X mouse equivalent doses (MED) for up to two weeks did not elicit significant histomorphological, physiological, biochemical or molecular alterations in mouse livers. At the same time, administration of dGTE at MED comparable to those consumed by humans resulted in significant modulation of gut microflora, with increases in Akkermansia sp. being most pronounced. Results of this study demonstrate that administration of relevant-to-human-consumption MED of dGTE to non-fasting mice does not lead to hepatotoxicity. Furthermore, dGTE administered to lean mice, caused changes in gut microflora comparable to those observed in obese mice. This study provides further insight into the previously reported weight management properties of dGTE; however, future studies are needed to fully evaluate and understand this effect. Full article
(This article belongs to the Special Issue Nutraceutical, Nutrition Supplements and Human Health)
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