Protective effect of hawthorn extract against genotoxicity induced by benzo(<alpha>)pyrene in C57BL/6 mice

Abstract

Benzo(<alpha>)pyrene [B(<alpha>)P], widely originated from environmental pollution or food process such as roasting and frying, is a strong mutagen and potent carcinogen. Utilization of hawthorn has been reported against physical mutagens. Our study found that hawthorn extract (HE) contained abundant phenolic compounds, wherein chlorogenic acid was 2.78 mg/g, procyanidine B2 was 3.58 mg/g, epicatechin was 2.99 mg/g DW, which may contribute to anti-genotoxicity activity. So, the role of HE against B(<alpha>)P-induced genotoxicity in C57BL/6 mice was further assessed. Fifty mice were distributed into five groups: control group, B(<alpha>)P group (30 mg/kg, i.p.), B(<alpha>)P + HE-L group (100 mg/kg, i.g.), B(<alpha>)P + HE-M group (200 mg/kg, i.g.), B(<alpha>)P + HE-H group (400 mg/kg, i.g.). Mice were orally administered with solutions of HE for 10 days and injected intraperitoneally with B(<alpha>)P for 3 days from the 8th day. Results showed that B(<alpha>)P can induce significantly pathological damage in liver, lung and spleen, as well as decrease white blood cells (WBCs). Remarkably elevated levels of reactive oxygen species (ROS), DNA strand breaks (DSBs) and G1 cell cycle arrest were also found in B(<alpha>)P group, with upregulated expressions of p-H2AX, p-p53 and p21 in bone marrow cells. With administration of HE, liver, lung and spleen injury significantly mitigated, while WBCs were evidently increased in B(<alpha>)P-treated mice. Consistently, HE markedly reduced level of ROS, DSBs and G1 cell cycle arrest accompanied by reducing expressions of p-H2AX, p-p53 and p21 in bone marrow cells. Combined, these results indicated a protective role of HE on B(<alpha>)P-induced genotoxicity.

Keywords: Antioxidant; Benzo()pyrene; Cell cycle arrest; DNA strand breaks; Genotoxicity; Hawthorn extract.