Institute of Mitochondrial Biology and Medicine
Institute of Mitochondrial Biology and Medicine
Feng Z.,Institute of Mitochondrial Biology and Medicine |
Feng Z.,CAS Shanghai Institutes for Biological Sciences |
Jia H.,CAS Shanghai Institutes for Biological Sciences |
Li X.,CAS Shanghai Institutes for Biological Sciences |
And 10 more authors.
Neurochemical Research | Year: 2010
Lycium barbarum (Fructus Lycii, Wolfberry, or Gouqi) belongs to the Solanaceae. The red-colored fruits of L. barbarum have been used for a long time as an ingredient in Chinese cuisine and brewing, and also in traditional Chinese herbal medicine for improving health. However, its effects on cognitive function have not been well studied. In the present study, prevention of a milkbased wolfberry preparation (WP) on cognitive dysfunction was tested in a prenatal stress model with rats and the antioxidant mechanism was tested by in vitro experiments. We found that prenatal stress caused a significant decrease in cognitive function (Morris water maze test) in female offspring. Pretreatment of the mother rats with WP significantly prevented the prenatal stress-induced cognitive dysfunction. In vitro studies showed that WP dose-dependently scavenged hydroxyl and superoxide radicals (determined by an electron spin resonance spectrometric assay), and inhibited FeCl2/ascorbic acid-induced dysfunction in brain tissue and tissue mitochondria, including increases in reactive oxygen species and lipid peroxidation and decreases in the activities of complex I, complex II, and glutamate cysteine ligase. These results suggest that dietary supplementation with WP may be an effective strategy for preventing the brain oxidative mitochondrial damage and cognitive dysfunction associated with prenatal stress. © Springer Science+Business Media, LLC 2010.
Gao M.,Institute of Mitochondrial Biology and Medicine |
Li Y.,Xi'an Technological University |
Xue X.,PLA Fourth Military Medical University |
Long J.,Institute of Mitochondrial Biology and Medicine |
And 3 more authors.
Asian Pacific Journal of Cancer Prevention | Year: 2014
This study was to undertaken to investigate the impacts of AhR, CYP1A1, GSTM1 genetic polymorphisms on the R273G mutation in exon 8 of the tumor suppressor p53 gene (TP53) among polycyclic aromatic hydrocarbons (PAHs) exposed to coke-oven workers. One hundred thirteen workers exposed to PAH and 82 control workers were recruited. We genotyped for polymorphisms in the AhR, CYP1A1, GSTM1, and TP53 R273G mutation in blood by PCR methods, and determined the levels of 1-hydroxypyrene as PAH exposure marker in urine using the high pressure liquid chromatography assay. We found that the distribution of alcohol users and the urinary excretion of 1-OHP in the exposed workers were significantly higher than that of the control workers (p=0.004, p<0.001, respectively). Significant differences were observed in the p53 genotype distributions of smoking subjects (p=0.01, 95%CI: 1.23-6.01) and PAH exposure (p=0.008, 95%CI: 1.24-4.48), respectively. Further, significant differences were observed in the p53 exon 8 mutations for the genetic polymorphisms of Lys/Arg for AhR (p=0.02, 95%CI: 0.70-15.86), Val/Val for CYP1A1 (p=0.04, 95%CI: 0.98-19.09) and null for GSTM1 (p=0.02, 95%CI: 1.19-6.26), respectively. Our findings indicated that polymorphisms of PAH metabolic genes, such as AhR, CYP1A1, GSTM1 polymorphisms may interact with p53 genetic variants and may contribute to PAH related cancers.
Chen W.,Chinese Academy of Sciences |
Liu X.,Northwest University, China |
Shi J.,Northwest University, China |
Zheng Y.,Chinese Academy of Sciences |
And 2 more authors.
Food Chemistry | Year: 2010
Betel quid chewing is a widely prevalent habit correlated with a high incidence of oral cancer. However, the underlying mechanism of the carcinogenicity of betel quid chewing is poorly understood. In the present study, the carcinogenic mechanism of action of betel quid chewing was examined by determining DNA damage induced by arecaidine and Cu(II). It was found that arecaidine alone had no significant effect on inducing DNA damage, but it caused significant DNA double stand breaks in the presence of Cu(II) ions under alkaline conditions. Further studies showed that reactive oxygen species were generated and Cu(I) was formed in the reaction. The arecaidine anion exhibited a lower IP and a higher HOMO energy than arecaidine itself, suggesting an increased ability to donate electrons under alkaline pH conditions. These results suggest that the presence of Cu(II) and alkaline conditions are two essential factors in arecaidine-induced DNA damage, a contributing factor to oral cancer occurrence. © 2009 Elsevier Ltd. All rights reserved.