**1. Introduction**

Liver cancer is the third most common cause of cancer mortality worldwide especially in developing countries. Epidemiological studies among all continents found that Asia and Africa have higher incidence rate than western world [1]. Hepatocellular carcinoma (HCC), arise due to excessive growth of abnormal liver cells, is most commonly found among all liver cancer types [2]. Four main potential causes of HCC have been identified as viral infection (chronic hepatitis B and C), metabolic syndrome (diabetes and nonalcoholic fatty liver disease), immune-related disease (autoimmune hepatitis), and toxic substances (alcohol and aflatoxins) [3].

Aflatoxin B1 (AFB1) is a noxious carcinogen produced by certain fungi *Aspergillus flavus* and *A. parasiticus* which mostly contaminate in agricultural products such as rice, chili, and peanuts. AFB1 is a Class 1 carcinogen classified by the International Agency for Research on Cancer (IARC), suggesting sufficient evidence of carcinogenicity caused by AFB1 in both animals and human [4]. Consequently, it is considered as a serious contaminant in many foodstuffs.

Once the AFB1 is absorbed through human body, it is metabolized at the liver site by phase I metabolizing enzymes including hydroxylation, hydration, demethylation, and epoxidation. Nontoxic metabolites are resulted from hydroxylation, hydration, and demethylation while the reactive metabolite, AFB1-8,9-epoxide, is resulted from epoxidation [3, 4]. AFB1-8,9-epoxide is the genotoxic form and can react efficiently with DNA at the N7 site of guanine to form AFB1 adduct. This adduct can adversely affect DNA sequence and genetic materials. However, human defensive mechanisms are able to detoxify AFB1 toxicity through phase II metabolism enzymes. AFB1 can be converted into excretable forms after binding with glutathione and glucuronic acid generated by specific enzyme, glutathione S-transferase (GST) and UDP-glucuronosyltransferase (UGT), respectively [5–7]. Besides acute toxicity such as hepatic necrosis, bile drug proliferation, edema, and lethargy could also be observed after exposure to high dose of AFB1 [8].

Regarding the current situation, there are many ways to avoid the risk of AFB1 induced liver cancer as determined by two main periods, pre- and post-harvest period and exposure period [6]. During harvest time, several techniques are used for controlling and reducing the chance of harmful effects resulted from AFB1: cultivation of AFB1 tolerance plants, biocontrol using competitive fungi, irrigation, and insecticide. For exposure period, most researches aim to determine the effects of several foods or supplementary foods that are capable of decreasing AFB1 induced toxicity. For example, oltipraz, a synthetic derivative of natural compound originated from cruciferous vegetables, is reported on its capacity to reduce AFB1 toxicity. In addition, green tea polyphenol and chlorophyllin (a derivative of chlorophyll found in green leafy vegetables) are also stated. These natural compounds have a potential against AFB1-induced hepatocarcinogenicity by decreasing the absorption of AFB1, controlling metabolic pathway, and increasing AFB1 excretion [6, 9]. To update the involvement of edible plants as chemoprevention for AFB1, this review is aimed to emphasize the mechanistic alleviation of AFB1-induced liver toxicity by polyphenol-containing plants.
