Protective effect of sulforaphane pretreatment against cisplatin-induced liver and mitochondrial oxidant damage in rats

Gaona-Gaona, Leobardo; Molina‐Jijón, Eduardo; Tapia, Edilia; Zazueta, Cecilia; Hernández-Pando, Rogelio; Calderón‐Oliver, Mariel; Zarco-Márquez, Guillermo; Pinzón, Enrique; Pedraza‐Chaverrí, José

doi:10.1016/j.tox.2011.04.014

Cited by 109 publications

(61 citation statements)

References 51 publications

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“…It has been proposed that the induction of the nuclear translocation of Nrf2 and its binding to the antioxidant response element (ARE), whereby the cytoprotective genes transcription is activated, may occur either by disruption of interactions between Nrf2 and Kelch-like ECH-associated protein 1 (Keap 1) or by mitogen-activated protein kinases (MAPK) pathways activation (Vasanthi et al 2009;Dinkova-Kostova & Kostov 2012;Guerrero-Beltran et al 2012). Therefore, SFN is classified as an indirect antioxidant which scavenging ability for several ROS is very low or negligible (Gaona-Gaona et al 2011). Noh et al (2015) treated male mice with APAP (300 mg/kg) 30 min after SFN administration (5 mg/kg).…”

Section: Silymarinmentioning

confidence: 99%

Role of food-derived antioxidant agents against acetaminophen-induced hepatotoxicity

Eugenio‐Pérez

Oca-Solano

Pedraza‐Chaverrí

2016

Pharmaceutical Biology

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Context Acetaminophen (APAP), also known as paracetamol and N-acetyl p-aminophenol, is one of the most frequently used drugs for analgesic and antipyretic purposes on a worldwide basis. It is safe and effective at recommended doses but has the potential for causing hepatotoxicity and acute liver failure (ALF) with overdose. To solve this problem, different strategies have been developed, including the use of compounds isolated from food, which have been studied to characterize their efficacy as natural dietary antioxidants. Objective The objective of this study is to show the beneficial effects of a variety of natural compounds and their use against acetaminophen-induced hepatotoxicity. Methods PubMed database was reviewed to compile data about natural compounds with hepatoprotective effects against APAP toxicity. Results and conclusion As a result, the health-promoting properties of 13 different food-derived compounds with protective effect against APAP-induced hepatotoxicity were described as well as the mechanisms involved in hepatoprotection.ARTICLE HISTORY

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Section: Silymarinmentioning

confidence: 99%

Role of food-derived antioxidant agents against acetaminophen-induced hepatotoxicity

Eugenio‐Pérez

Oca-Solano

Pedraza‐Chaverrí

2016

Pharmaceutical Biology

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“…Nothing was given to the control group throughout the experiment. SFN was administered for treatment via oral gavage at a dose of 500 μg/kg for three days to the rats of SFN and APAP+SFN groups (15). Acetaminophen was dissolved in hot saline and administered on the third day to produce toxic hepatitis via a single oral gavage at a dose of 1 g/kg to the rats of the APAP and APAP+SFN groups (16).…”

Section: Experimental Groupsmentioning

confidence: 99%

“…To the best of our knowledge, there are very few studies investigating the effects of sulforaphan on acetaminophen-induced hepatotoxicity (26). Gaona-Gaona et al (15) experimentally induced liver damage and reported that sulforaphane reduced the MDA levels in the liver by decreasing lipid peroxidation. In our study, we determined that sulforaphane signifi cantly decreased liver MDA levels in the treatment group compared to the hepatotoxicity group.…”

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confidence: 99%

“…Besides, increased neopterin levels may be also responsible for the development of irreversible hepatocellular damage (51). Gaonae Gaona L et al (15) reported that sulforaphane exhibits its hepatoprotective effects by protecting mitochondrial function and antioxidant enzymes and by preventing mitochondrial oxidative stress in the liver. There is no study in the literature showing the effects of sulforaphane on neopterin levels in experimental liver damage.…”

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confidence: 99%

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The effect of sulforaphane on oxidative stress and inflammation in rats with toxic hepatitis induced by acetaminophene

Dokumacıoğlu¹,

İskender²,

Aktaş³

et al. 2017

BLL

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OBJECTIVE: The aim of the present study was to reveal the possible effect of sulforaphane on oxidative stress and infl ammation in rats liver with toxic hepatitis induced by acetaminophene. BACKGROUND: Sulforaphane is a compound with high antioxidant properties. Acetaminophen, which is a para-aminophenol derivative, can lead to fatal hepatic necrosis with direct hepatotoxic effects at high doses. METHODS: Thirty six male Sprague-Dawley rats were randomly divided into four groups. Control group (n = 9) was fed with standard rat chow and water for 3 days. Group APAP (n = 9) received a single dose acetaminophen 1 g/kg by oral gavage in addition to standard chow and water. Group SFN (n = 9) received sulforaphane 500 μg/kg by oral gavage in addition to standard chow and water for 3 days. Group APAP+SFN (n = 9) received sulforaphane 500 μg/kg and a single dose acetaminophen 1 g/kg by oral gavage in addition to standard chow and water. Acetaminophen was administered three hours after SFN administration. RESULTS: Neopterin, MDA, AST, ALT and CRP levels of group APAP were signifi cantly increased compared to control group. GSH level of group APAP was signifi cantly lower than in the control group. CONCLUSION: Sulforaphane is a protective agent against acetaminophen-induced liver damage and it can be added in the treatment protocol (Tab. 1, Fig. 5, Ref. 51). Text in PDF www.elis.sk.

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“…However, the cellular mechanisms of testicular injury caused by cisplatin were poorly understood. Several studies have shown that pathogenesis of renal, hepatic, testicular damage following CDDP exposure is generally ascribed to oxidative damage (Chirino, Pedraza-Chaverri, 2009;Gaona-Gaona et al, 2011;Ahmed et al, 2011), in addition, an increase in apoptotic rate of germ cell is seen because of the side effects of cisplatin (Amin et al, 2008;Lirdi et al, 2008) .…”

Section: Introdutionmentioning

confidence: 99%

Anti-apoptotic Effect of Grape Seed Proanthocyanidin Extract on Cisplatin-induced Apoptosis in Rat Testis

Zhao

Hai-lian

Gao

2015

FSTR

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Protective effect of sulforaphane pretreatment against cisplatin-induced liver and mitochondrial oxidant damage in rats

Cited by 109 publications

References 51 publications

Role of food-derived antioxidant agents against acetaminophen-induced hepatotoxicity

Role of food-derived antioxidant agents against acetaminophen-induced hepatotoxicity

The effect of sulforaphane on oxidative stress and inflammation in rats with toxic hepatitis induced by acetaminophene

Anti-apoptotic Effect of Grape Seed Proanthocyanidin Extract on Cisplatin-induced Apoptosis in Rat Testis

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