Hepatotoxicity is the most widespread pathology worldwide, representing up to 83% of all cases. Hepatitis, viral infections, food additives, alcohol, toxic industrial chemicals, and air and water pollutants are the major risk factors of liver toxicity. There is increasing evidence that free radicals and reactive oxygen species play a crucial role in various steps that initiate and regulate the progression of liver diseases independently of the original agent . Carbon tetrachloride (CCl4) is a potent environmental hepatotoxin  that, in addition to hepatic problems, causes dysfunction of the kidneys, lungs, testis, brain, and blood by generating free radicals [3, 4].
CCl4 requires bioactivation in phase I of the cytochrome P450 system to form the reactive metabolic trichloromethyl radical (·CCl3) and trichloromethyl peroxy radical (·OOCCl3). These free radicals can bind with polyunsaturated fatty acids to produce alkoxy (R·) and peroxy radicals (ROO·) that, in turn, generate lipid peroxides that are highly reactive, change enzyme activity, and finally induce injury or necrosis with corresponding health problems [5, 6].
CCl4 is known to decrease glutathione (GSH) of phase II enzymes and reduce antioxidant enzymes and substrates to induce oxidative stress, which is an important factor in acute and chronic injuries in various tissues [7, 8]. Free radicals of CCl4 reduce the GSH contents and activities of antioxidant enzymes, leading to hepatic injury . The depletions of these antioxidant enzymes occur secondary to the controlling action against peroxy radicals produced by CCl4. Reactive oxygen species cause oxidative DNA damage in the form of DNA adducts, genetic mutation, strand breakage, and chromosomal alterations . Some recent investigations revealed that free radicals increased the number of argyrophilic nucleolar organizer regions (AgNORs) and activity of telomerase in kidney tissues , caused depletion of cytochrome P450 2E1, and increased the 8-hydroxyl-2 deoxyguanosine concentration . DNA fragmentation causes p53 gene expression, blocks the cell cycle, and gives additional time to repair DNA. However, severe DNA damage triggers apoptosis .
Sonchus asper (SAME), locally called Mahtari, is a common herb that grows wildly and abundantly in open fields. Chemical studies of SAME indicated a high content of vitamin C (ascorbic acid) , carotenoids, and type ω-3 fatty acids [15, 16]. Phenolic compounds, which are secondary metabolites in plants, are one of the most widely occurring groups of phytochemicals that exhibit a wide range of physiological properties, such as antioxidant, anti-allergenic, anti-microbial, anti-artherogenic, anti-thrombotic, anti-inflammatory, vasodilatory, and cardioprotective effects [17, 18]. Chemical characterization of SAME has shown the presence of ionone derivatives of glycosides and sesquiterpene lactone glycosides . These bioactive compounds have been shown to possess strong antioxidant and anti-inflammatory properties . SAME has diuretic, refrigerant, sedative, and antiseptic properties that are used in the treatment of cough, bronchitis, and asthma  as well as kidney inflammation , and its decoction is used in the treatment of impotence (erectile dysfunction) . With increasing recognition of herbal medicine and phytotherapy as alternative forms of health care, the objectives of this study were to evaluate the antioxidant and hepatoprotective properties of SAME against CCl4-induced hepatic injuries in Sprague–Dawley male rats.