Highlights d Successful ovulation requires timely expression of PGR in the ovarian granulosa cells d PGR terminates LH-surge-driven PGE2 synthesis by decreasing PTGS2 (COX-2) expression d Impaired PGR expression leads to hyperinflammation and tissue damage in the ovary Authors

Topical application of caffeine sodium benzoate (caffeine-SB) immediately after UVB irradiation of SKH-1 mice enhanced UVB-induced apoptosis by a 2- to 3-fold greater extent than occurred after the topical application of an equimolar amount of caffeine. Although topical application of caffeine-SB or caffeine enhanced UVB-induced apoptosis, both substances were inactive on non-UVB-treated normal skin. Topical application of caffeine-SB or caffeine (each has UVB absorption properties) 0.5 h before irradiation with a high dose of UVB decreased UVB-induced thymine dimer formation and sunburn lesions (sunscreen effect). Caffeine-SB was more active than an equimolar amount of caffeine in exerting a sunscreen effect. In additional studies, caffeine-SB strongly inhibited the formation of tumors in UVB-pretreated 'high-risk mice' and in tumor-bearing mice, and the growth of UVB-induced tumors was also inhibited. Caffeine-SB and caffeine are the first examples of compounds that have both a sunscreen effect and enhance UVB-induced apoptosis. Our studies suggest that caffeine-SB and caffeine may be good agents for inhibiting the formation of sunlight-induced skin cancer.

No abstract

No abstract

Pyridoxamine, pyridoxine, and pyridoxal phosphate were tested to examine if they have antioxidant properties. Endothelial cells exposed to 0.5 mM H(2)O(2) for 2 hours increased the superoxide anion and lipid peroxide levels as biomarkers of oxidative stress. The increase of superoxide was mainly due to the activation of NADPH-oxidase by H(2)O(2). Preincubation of the endothelial cells with 0.1 or 1.0 mM of pyridoxamine or pyridoxal phosphate for one-half hour before H(2)O(2) exposure significantly reduced the superoxide and lipid peroxide compared to the cells exposed to H(2)O(2) only. Preincubation of the cells with 0.1 or 1.0 mM of pyridoxine also significantly reduced the lipid peroxide but did not significantly affect the superoxide level unless the preincubation time was extended to 24 hours. The prostacyclin release by endothelial cells was also significantly inhibited by H(2)O(2). However, the preincubation of endothelial cells with 1.0 mM of pyridoxamine, pyridoxine, or pyridoxal phosphate did not prevent that inhibition. These results indicate that pyridoxamine, pyridoxine, and pyridoxal phosphate acted as antioxidants and reduced the superoxide and lipid peroxides induced by H(2)O(2), but did not protect the cells from the effects directly related to H(2)O(2) itself.