Flavonoid-rich fraction attenuates permethrin-induced toxicity by modulating ROS-mediated hepatic oxidative stress and m
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RESEARCH ARTICLE
Flavonoid-rich fraction attenuates permethrin-induced toxicity by modulating ROS-mediated hepatic oxidative stress and mitochondrial dysfunction ex vivo and in vivo in rat Nissaf Aoiadni 1 & Houda Ayadi 2 & Hajer Jdidi 1 & Manel Naifar 3 & Sami Maalej 2 & Fatma Ayadi Makni 3 & Abdelfattah El Feki 1 & Hamadi Fetoui 4 & Fatma Ghorbel Koubaa 1 Received: 8 April 2020 / Accepted: 13 October 2020 # Springer-Verlag GmbH Germany, part of Springer Nature 2020
Abstract The present study explores the antioxidant, anti-microbial, and hepatoprotective potentials of flavonoid-rich fractions from Fumaria officinalis against permethrin-induced liver damage ex vivo/in vivo in rat. However, HPLC-DAD analysis revealed the richness of 6 components in ethyl acetate fraction (EAF) where ferulic acid, rosmarinic acid, and myricetin are the most abundant. The in vitro assays showed that EAFs have impressive antioxidant and anti-microbial properties. Ex vivo, permethrin (PER) (100 μM) induced a decrease of hepatic AST and ALT activities and 25-OH vitamin D and vitamin C levels and an increase of ALP and LDH activities, TBARS, and ϒ-GT levels with a disturbance of oxidative status. The hepatoprotective effect of EAF (1 mg/mL) against PER was confirmed by the amelioration of oxidative stress profile. In vivo, permethrin was found to increase absolute and relative liver weights, plasma transaminase activities, lactate-to-pyruvate ratio, hepatic and mitochondrial lipid peroxidation, and protein oxidation levels. This pesticide triggered a decrease of Ca2+ and Mg2+-ATPases and mitochondrial enzyme activities. The co-treatment with EAF reestablished the hepatic and mitochondrial function, which could be attributed to its richness in phenolic compounds. Keywords Fumaria officinalis . Flavonoid . Liver . Mitochondria . Permethrin
Introduction Liver is a vital organ in the processes of drugs and xenobiotic metabolism and detoxification (Sahreen et al. 2011). Sometimes, toxic substances are converted during these processes to active metabolites that can cause hepatic damage Responsible Editor: Mohamed M. Abdel-Daim * Nissaf Aoiadni [email protected] 1
Laboratory of Animal Eco-Physiology, Faculty of Sciences of Sfax, Street of Soukra Km 3.5, BP 1171, CP 3000 Sfax, Tunisia
2
Laboratory of Biodiversity and Aquatic Ecosystems, Ecology and Planktonology, Sciences Faculty of Sfax, Street of Soukra Km 3.5, BP 1171, CP 3000 Sfax, Tunisia
3
Laboratory of Biochemistry, CHU Habib Bourguiba, Sfax, Tunisia
4
Laboratory of Toxicology and Environmental Health.LR17ES06, Sciences Faculty of Sfax, University of Sfax, BP1171, 3000 Sfax, Tunisia
(Cullen 2005). The risk of liver injury has significantly been associated with the metabolic dysfunctions that can result in various disorders ranging from an ephemeral elevation of liver enzymes to life-threatening hepatocellular carcinoma (HCC). HCC is one of the most frequent tumors representing the fifth commonest malignancy worldwide and the third cause of mortality from cancer accountin
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