BackgroundA sedentary lifestyle and poor diet are risk factors for the progression of non-alcoholic fatty liver disease. However, the pathogenesis of hepatic lipid accumulation is not completely understood. Therefore, the present study explored the effects of dietary supplementation of various ratios of docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) on a high-fat diet-induced lipid metabolism disorder and the concurrent liver damage.MethodsUsing high-fat diet-fed C57BL/6 J mice as the animal model, diets of various ratios of DHA/EPA (2:1, 1:1, and 1:2) with an n-6/n-3 ratio of 4:1 were prepared using fish and algae oils enriched in DHA and/or EPA and sunflower seed oils to a small extent instead of the high-fat diet.ResultsSignificantly decreased hepatic lipid deposition, body weight, serum lipid profile, inflammatory reactions, lipid peroxidation, and expression of adipogenesis-related proteins and inflammatory factors were observed for mice that were on a diet supplemented with DHA/EPA compared to those in the high-fat control group. The DHA/EPA 1:2 group showed lower serum triglycerides (TG), total cholesterol (TC), and low-density lipoprotein-cholesterol levels, lower SREBP-1C, FAS, and ACC-1 relative mRNA expression, and higher Fra1 mRNA expression, with higher relative mRNA expression of enzymes such as AMPK, PPARα, and HSL observed in the DHA/EPA 1:1 group. Lower liver TC and TG levels and higher superoxide dismutase levels were found in the DHA/EPA 2:1 group. Nonetheless, no other notable effects were observed on the biomarkers mentioned above in the groups treated with DHA/EPA compared with the DHA group.ConclusionsThe results showed that supplementation with a lower DHA/EPA ratio seems to be more effective at alleviating high-fat diet-induced liver damage in mice, and a DHA/EPA ratio of 1:2 mitigated inflammatory risk factors. These effects of n-3 polyunsaturated fatty acids (PUFA) on lipid metabolism may be linked to the upregulation of Fra1 and attenuated activity of c-Jun and c-Fos, thus ultimately reducing the severity of the lipid metabolism disorder and liver damage to some extent.

Heat shock protein 70 (Hsp70) comprises proteins that have been reported to protect cells, tissues, and organisms against damage from a wide variety of stressful stimuli; however, little is known about whether Hsp70 protects against DNA damage. In this study, we investigated the relationship between Hsp70 expression and the levels of ultraviolet C (UVC)-induced DNA damage in A549 cells with normal, inhibited, and overexpressed Hsp70 levels. Hsp70 expression was inhibited by treatment with quercetin or overexpressed by transfection of plasmids harboring the hsp70 gene. The level of DNA damage was assessed by the comet assay. The results showed that the levels of DNA damage (shown as the percentage of comet cells) in A549 cells increased in all cells after exposure to an incident dose of 0, 10, 20, 40, and 80 J/m2 whether Hsp70 was inhibited or overexpressed. This response was dose dependent: a protection against UVC-induced DNA damage in cells with overexpressed Hsp70 was observed at UVC dose 20 J/m2 with a maximum at 40 J/m2 when compared with cells with normal Hsp70 levels and in quercetin-treated cells. This differential protection disappeared at 80 J/m2. These results suggest that overexpressed Hsp70 might play a role in protecting A549 cells from DNA damage caused by UVC irradiation, with a threshold of protection from at UVC irradiation-induced DNA damage by Hsp70. The detailed mechanism how Hsp70 is involved in DNA damage and possible DNA repair warrants further investigation.

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N,N′-Dinitrosopiperazine (DNP) induces nasopharyngeal carcinoma (NPC) and shows organ specificity to the nasopharyneal epithelium. To investigate its mechanism, the rat NPC model was inducd using DNP. Rat NPC and normal nasopharyngeal cells were obtained from the NPC model using laser capture. The total proteins from these cell samples were separated with two-dimension polyacrylamide gel electrophoresis techniques, and highly expressed proteins (> five-fold) were analyzed using matrix-assisted laser desorption/ionization time of flight and bioinformatics. The results showed that HSP70 and mucin 5B expression increased not only in rat NPC but also in atypical hyperplasia nasopharyngeal tissues, a precancer stage of NPC. High-expression of heat shock protein 70 (HSP70) and mucin 5B was further supported by western blot analysis. T he nonviral exposure most consistently and strongly associated with risk of nasopharyngeal carcinoma (NPC) is the consumption of salt-preserved fish, a traditional staple food in several NPC-endemic areas.(1) In studies of Chinese populations, the relative risk of NPC is associated with weekly consumption, compared with no or rare consumption which has been shown to range from 1.4 to 3.2, whereas that for daily consumption has been shown to range from 1.8 to 7.5.However, NPC risk is also elevated in association with other preserved food items, including meats, eggs, fruits, and vegetables. (4)(5)(6)(7)(8)(9)(10)(11)(12)(13)(14)(15) In southern China, intake of salted and other preserved foods is particularly high among boat-dwelling fishermen and their families, known as Tankas-the population subgroup at highest risk of developing NPC. Salt-preserved foods are a dietary staple in all NPC-endemic populations. (14,16) Furthermore, salted fish is a traditional weaning food, resulting in early and frequent feeding of infants-especially in the Cantonese population (4,14) and in families of lower socioeconomic status. (3,17) Childhood exposure, especially at weaning seems more strongly related to NPC risk than adulthood exposure. (3,4,(14)(15)(16)(18)(19)(20) This dietary pattern may explain part of the international distribution of NPC incidence.The carcinogenic potential of salt-preserved fish is supported by experiments in rats, which develop malignant nasal and NPC.(21-23) The process of salt preservation is inefficient, allowing fish and other foods to become partially putrefied. (24,25) As a result, these foods accumulate significant levels of nitrosamines, which are known as carcinogens.(24,26-28) Consumption of salted fish is an important source of nitrosamines. NNitrosodimethylamine is the predominant volatile nitrosamine in salted fish. After enzymatic metabolic or bacteria activation, N-nitrosodimethylamine forms an important carcinogenic N-nitroso compounds. (25) In some experiments in rats, the carcinogenecity of nitrosamines and N-nitroso compounds has been proved, for instance diethylnitrosamine (DNE), dimethlbenzanthracene-anthracene (DMBA), and DNP. (6,15,29) In our previous s...

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