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Abstract: The aim of the present study was to assess the protective effect of apigenin, a dietary flavone, against cytogenetic alterations in human peripheral blood lymphocytes (HPBL) induced by Cobalt-60 radiation (3Gy). Results of MTT [3-(4, 5-dimethyl-2-thiaozolyl)-2,5-diphenyl-2H tetrazolium bromide] assay revealed that 37.2μM of apigenin was found to be non-toxic in HPBL. At this dose (37.2μM) of apigenin, the LD50 radiation dose of HPBL increased from 2.9Gy to 3.4Gy, which resulted in a DMF of 1.17. Apigenin (37.2μM) treatment 1h before irradiation significantly (p <0.05) reduced DNA damage in irradiated HPBL as measured by comet assay (% tail DNA, tail length, tail moment, and olive tail moment). Moreover, apigenin treatment significantly decreased the frequencies of dicentric (DC), acentric fragments (AF), and acentric rings (AR) in irradiated HPBL. Apigenin pretreatment also reduced the radiation-induced CBMN (cytokinesis blocked micronuclei) anomalies such as micronuclei (MNi), nucleoplasmic bridges (NPB) and nuclear buds (NBUD) in HPBL. These results also showed that there was a significant correlation between NPB and DC frequencies and MNi and AF+AR. Treatment with apigenin alone had no significant effect on DNA damage and chromosomal aberrations in HPBL. Thus, the current studies indicate that apigenin protects HPBL from radiation-induced cytogenetic alterations. [Copyright &y& Elsevier]

Abstract: The present study was aimed to explore the antioxidant potential of apigenin and its preventive effect on radiation-induced oxidative damage in human peripheral blood lymphocytes (HPBL). Apigenin (4′, 5, 7-trihydroxy flavone) effectively scavenges hydroxyl (OH•), superoxide anion (O2 •–), 1, 1-diphenyl- 2-picrylhydrazyl (DPPH•) in a concentration-dependent manner (37.2–186μM). Gamma-radiation (3Gy) exposure increased the levels of reactive oxygen species (ROS), % apoptotic cells and decreased the mitochondrial membrane potential (ΔΨm) in HPBL. On the other hand, apigenin treatment (37.2μM) 60min prior to irradiation significantly decreased ROS generation in HPBL. It has also been observed that apigenin treatment significantly reduced γ-radiation-induced apoptotic incidence and modulates loss of ΔΨm in HPBL. Furthermore, apigenin treatment significantly maintains cellular antioxidant status (superoxide dismutase, catalase, glutathione peroxidase activities and reduced glutathione level) and protects cellular milieu from γ-radiation-induced lipid peroxidation and micronuclei formation in irradiated HPBL. Radiation exposure increased p53, p21, Bax and NF-kB expressions and decreased Bcl-2 expression in HPBL. Conversely, an increase in Bcl-2 along with a decrease in p53, p21, Bax and NF-kB expression was observed in apigenin plus irradiated HPBL. Taken together, the present study indicates that apigenin showed strong antioxidant property in free radical scavenging systems and protects HPBL from radiation-induced oxidative damages at cellular and molecular level. [Copyright &y& Elsevier]•+) in a concentration-dependent manner (37.2–186μM). Gamma-radiation (3Gy) exposure increased the levels of reactive oxygen species (ROS), % apoptotic cells and decreased the mitochondrial membrane potential (ΔΨm) in HPBL. On the other hand, apigenin treatment (37.2μM) 60min prior to irradiation significantly decreased ROS generation in HPBL. It has also been observed that apigenin treatment significantly reduced γ-radiation-induced apoptotic incidence and modulates loss of ΔΨm in HPBL. Furthermore, apigenin treatment significantly maintains cellular antioxidant status (superoxide dismutase, catalase, glutathione peroxidase activities and reduced glutathione level) and protects cellular milieu from γ-radiation-induced lipid peroxidation and micronuclei formation in irradiated HPBL. Radiation exposure increased p53, p21, Bax and NF-kB expressions and decreased Bcl-2 expression in HPBL. Conversely, an increase in Bcl-2 along with a decrease in p53, p21, Bax and NF-kB expression was observed in apigenin plus irradiated HPBL. Taken together, the present study indicates that apigenin showed strong antioxidant property in free radical scavenging systems and protects HPBL from radiation-induced oxidative damages at cellular and molecular level. [Copyright &y& Elsevier]

Exposure to solar ultraviolet-B (UVB) radiation leads to the formation of cyclobutane pyrimidine dimers (CPDs). We investigated the protective effect of apigenin against UVB-induced CPDs formation in human dermal fibroblasts cells (HDFa). For this purpose, HDFa cells were treated with apigenin (15 μM) prior to UVB irradiation (20 mJ/cm 2 ); DNA damage and subsequent molecular end points were observed. Exposure to UVB radiation increased significant CPDs formation in HDFa cells and the frequencies of CPDs were reduced by treatment with apigenin (15 μM). UVB-induced CPDs downregulates the expression of nucleotide excision repair (NER) genes such as xeroderma pigmentosum complementation group C, B, G and F (XPC, XPB, XPG and XPF), transcription factor II human (TFIIH) and excision repair cross-complementation group 1 (ERCC1) in HDFa cells. Conversely, apigenin treatment restored UVB-induced loss of NER proteins in HDFa cells, which indicates its preventive effect against CPDs formation. Besides, single low dose UVB-exposure induced nuclear fragmentation, apoptotic frequency and apoptotic proteins expression (Bax and Caspase-3) have been prevented by the apigenin pretreatment. Furthermore, apigenin exhibits strong UV absorbance property and showed 10.08 SPF value. Thus, apigenin can protect skin cells against UVB-induced CPDs formation probably through its sunscreen effect. Hence, apigenin can be considered as an effective protective agent against UV induced skin damages. [ABSTRACT FROM AUTHOR]