Cantharidin-induced liver injuries in mice and the protective effect of vitamin C supplementation

Wu, Wei; Su, Min; Li, Taoming; Wu, Ka; Wu, Xinmou; Tang, Zhenxiang

doi:10.1016/j.intimp.2015.06.003

Cited by 24 publications

(27 citation statements)

References 27 publications

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“…However, this compound also has significant toxicity in mammals related to its anticancer activity (Deng et al, 2013; Puerto Galvis et al, 2013; Ratcliffe et al, 2014). Extensive studies have been undertaken to reduce this toxicity through modification of the compound (Deng et al, 2013; Puerto Galvis et al, 2013), alternative production and delivery methods (Chang et al, 2008; Han et al, 2013; Yu and Zhao, 2016), or combination therapies (Wu et al, 2015). These efforts highlight that the resolution of issues, such as toxicity, will require the investment of time and money into basic scientific research for the development process.…”

Section: Development Of Bioactive Molecules Into Therapeuticsmentioning

confidence: 99%

Tick Bioactive Molecules as Novel Therapeutics: Beyond Vaccine Targets

Murfin

Fikrig

2017

Front. Cell. Infect. Microbiol.

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Section: Development Of Bioactive Molecules Into Therapeuticsmentioning

confidence: 99%

Tick Bioactive Molecules as Novel Therapeutics: Beyond Vaccine Targets

Murfin

Fikrig

2017

Front. Cell. Infect. Microbiol.

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“…Its clinical application is still limited, although the effectiveness of cantharidin has been reported [20]. The main problem is toxicity, especially that causing liver injuries [21]. Cantharidin inhibited the proliferation of mesothelioma at 1 μM in an acidic medium [14], and ED50 in Ehrlich ascites carcinoma was approximately 130 μM in an alkaline medium used conventionally [22].…”

Section: Acidosis-dependent Anti-cancer Drugsmentioning

confidence: 99%

“…These results suggest that cantharidin can be used alone as an anti-cancer medicine. Vitamin C administration was reported to attenuate the liver injuries induced by cantharidin in mice [21], but the effect of vitamin C on anti-cancer therapy with cantharidin remains unclear. Derivatives of this drug have been synthesized to reduce the toxicity [26].…”

Section: Acidosis-dependent Anti-cancer Drugsmentioning

confidence: 99%

Cancer Chemotherapy Specific to Acidic Nests

Kobayashi

2017

Cancers

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The realization of cancer therapeutics specific to cancer cells with less of an effect on normal tissues is our goal. Many trials have been carried out for this purpose, but this goal is still far from being realized. It was found more than 80 years ago that solid cancer nests are acidified, but in vitro studies under acidic conditions have not been extensively studied. Recently, in vitro experiments under acidic conditions were started and anti-cancer drugs specific to acidic areas have been identified. Many genes have been reported to be expressed at a high level under acidic conditions, and such genes may be potent targets for anti-cancer drugs specific to acidic nests. In this review article, recent in vitro, in vivo, and clinical achievements in anti-cancer drugs with marked efficacy under acidic conditions are summarized, and the clinical use of anti-cancer drugs specific to acidic nests is discussed.

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“…Though cantharidin does not have targeted organs, its hepatotoxicity has attracted attention recently for the crucial role of the liver in detoxification. Cantharidin-induced liver damage was found in animals and humans who died of cantharidin intoxication (Chen & Huang, 2013;Han et al, 2013;Wu et al, 2015;Zhang et al, 2018;Zhu et al, 2019).…”

mentioning

confidence: 99%

“…To the best of our knowledge, previous studies were mainly focused on the effects of chronic cantharidin exposure on hepatotoxicity of animal models (Wu et al, 2015;Xiao et al, 2016;Zhu et al, 2019).…”

mentioning

confidence: 99%

Cantharidin‐induced acute hepatotoxicity: the role of TNF‐α, IKK‐α, Bcl‐2, Bax and caspase3

Zhang

et al. 2020

J of Applied Toxicology

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Cantharidin is of high medicinal value but has strong toxicity. Nowadays, multiple research has focused on the mechanism of its antitumor activity while research on toxicological profiles associated with cantharidin poisoning is still limited. Its hepatotoxicity has attracted attention recently for the crucial role of the liver in detoxification. Here, we aim to find a potential mechanism for cantharidin-induced acute hepatotoxicity with a view to assisting subsequent research or clinical use or detoxification. Twenty-one male Sprague-Dawley rats were randomly divided into control, low-dose (1.34 mg/kg) and high-dose (2.67 mg/kg) cantharidin exposure groups. We used hematoxylin-eosin to observe pathological changes and used immunofluorescent staining, western blotting and real-time quantitative polymerase chain reaction to detect the expression of the markers. The main pathological changes in livers of cantharidin-treated rats were necrosis, inflammatory infiltration and hemorrhage. We found coexpression of tumor necrosis factor alpha (TNF-α), IkappaB kinase-alpha (IKK-α) and caspase3 by immunofluorescent staining in livers of cantharidin-treated rats. Compared with the control, the levels of TNF-α, IKK-α and caspase3 increased significantly in the experimental groups (P < .05). The ratio of B-cell lymphoma-2 (Bcl-2)/Bax increased in the low-dose group but decreased in the high-dose group (P < .05). Cantharidin exposure raised IKK-α mRNA and caspase3 mRNA levels (P < .05). In conclusion, the participation of TNF-α, IKK-α, Bcl-2, Bax and caspase3 uncovered a novel mechanism underlying cantharidin-induced acute hepatotoxicity, and the mechanism needs to be studied further.

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Cantharidin-induced liver injuries in mice and the protective effect of vitamin C supplementation

Cited by 24 publications

References 27 publications

Tick Bioactive Molecules as Novel Therapeutics: Beyond Vaccine Targets

Tick Bioactive Molecules as Novel Therapeutics: Beyond Vaccine Targets

Cancer Chemotherapy Specific to Acidic Nests

Cantharidin‐induced acute hepatotoxicity: the role of TNF‐α, IKK‐α, Bcl‐2, Bax and caspase3

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