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Abstract: Exposure to ultraviolet B (UVB, 280–320) radiation induces the formation of reactive oxygen species (ROS) in the biological system. In this study, we examined the protective effect of ursolic acid on UVB-induced lipid peroxidation and oxidative DNA damage with reference to alterations in cellular antioxidant status in human lymphocytes. Series of in vitro tests (hydroxyl radical, superoxide, nitric oxide, DPPH and ABTS radical scavenging assays) demonstrates antioxidant property of ursolic acid in our study. Treatment of lymphocytes with ursolic acid alone (at 10μg/mL) gave no significant change in cell viability, thiobarbituric acid reactive substances (TBARSs), lipid hydroperoxides (LHPs), % tail DNA and tail moment when compared with normal lymphocytes. UVB-exposure significantly increased TBARS, LHP and % tail DNA, tail moment; decreased % cell viability and antioxidant status in irradiated lymphocytes. Treatment with ursolic acid 30min prior to UVB-exposure resulted in a significant decline of TBARS, LHP, % tail DNA and tail moment and increased % cell viability as ursolic acid concentration increased. Based on our results we conclude that ursolic acid, a dietary antioxidant, mediates its protective effect through modulation of UVB-induced reactive oxygen species. [Copyright &y& Elsevier]

Abstract: Sesamol pretreated (1, 5 and 10μg/ml) lymphocytes were exposed to different doses of γ-radiation, i.e., 1, 2 and 4Gray (Gy) and the cellular changes were estimated by using cytokinesis blocked micronucleus assay (MN), dicentric aberration (DC), thiobarbituric acid reactive substances (TBARS), reduced glutathione (GSH) and the activities of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx). Radiation significantly increased MN, DC frequencies, TBARS levels and decreased GSH and antioxidant enzyme levels in a dose dependent manner. The highest damage to lymphocytes was observed at 4Gy irradiation. On the other hand, sesamol pretreatment significantly decreased MN, DC frequencies, TBARS levels and increased GSH levels and SOD, CAT and GPx activities in a concentration dependent manner. At 1Gy irradiation all concentrations of sesamol (1, 5 and 10μg/ml) significantly protects the lymphocytes from radiation damage. At 2Gy irradiation 5 and 10μg/ml of sesamol shows significant radioprotection. Since the highest damage was observed at 4Gy irradiation both 1 and 5μg/ml of sesamol pretreatment were not sufficient to protect the lymphocytes from radiation damage but 10μg/ml of sesamol significantly (p <0.05) protects the lymphocytes from radiation effect. Thus, sesamol pretreatment gives significant protection to cultured human lymphocytes against γ-radiation induced cellular damage. The possible mechanism involved in the radioprotective influence of sesamol is discussed. [Copyright &y& Elsevier]

Highlights: [•] Antioxidant potential of Jatropha curcas. [•] UVB-radiation-induced DNA damage in cultured human blood lymphocytes. [•] RB4 fraction and L1 fraction protect UVB-radiation-induced DNA damage in HPBL. [ABSTRACT FROM AUTHOR]

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]