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The incidence rate of ovarian cancer ranks the third among female malignant tumors, the mortality rate ranks the first and the prognosis is poor. Ovarian cancer poses a serious threat to the health of women's lives. The incidence of ovarian cancer is related to heredity, endocrine disorders and adverse lifestyle factors. In recent years, some scholars have carried out the impact of lifestyle, especially shift work, on the occurrence and development of ovarian cancer. Shift work can lead to circadian disruption, which affects hormonal balance in the body and may be a risk factor for ovarian cancer. This review summarizes four cohort studies and two case-control studies on the relation between shift work and ovarian cancer. The conclusion of the studies is inconsistent, suggesting that further researches are needed.

Objective: To investigate the role of PPARα in oxidative damage of BRL-3A cells induced by perfluorooctanoic acid( PFOA) by inhibiting and activating gene expression., Methods: In vitro culture of rat liver BRL-3A cells were divided into blank control group, PFOA experimental control group, PPARα inhibition group( GW6471), PPARα agonist group( WY14643), PPARα inhibitor pretreatment PFOA group( GW6471 + PFOA), PPARα agonist pretreatment PFOA group( WY14643 + PFOA). Fluorescence immunocytochemistry was used to detect the expression of PPARα. The expression of PPARα and its downstream target gene was detected by q PCR. The expression of related protein was detected by Western blot., Results: The expression of PPARα in rat liver BRL-3A cells was successfully inhibited and stimulated by inhibitors and agonists( P < 0. 05). Compared with the blank control group and the PFOA experimental control group, there was a significant decrease in the content of ROS in the WY14643 + PFOA group compared with the blank control group and the PFOA experimental control group( P < 0. 05). The expression of PPARα and its downstream gene Cyp4a1 in GW6471 + PFOA group was higher than that in PPARα inhibitor group( P < 0. 05), but it was significantly lower than that in PFOA experimental control group( P < 0. 05). The expression of related genes in WY14643 + PFOA group was significantly lower than that in PPARα agonist group( P < 0. 05). The protein expression of PPARα in GW6471 + PFOA group was up-regulated compared with the inhibitor group, there was no difference compared with the blank control group. The protein expression of PPARα in WY14643 + PFOA group was not significantly different from that in agonist group, but it was significantly higher than that in PFOA experimental control group( P < 0. 05)., Conclusion: PFOA exposure can activate the expression of PPARα, remove ROS, PPARα played a protective role in PFOA-induced rat liver cell oxidative damage.

Objective: To study the effects on oxidative stress and the expression of PPARα-related genes and protein in the liver of rats induced by pentadecafluorooctanoic acid( PFOA)., Methods: A total of 28 male SD rats were randomly divided into four groups: control group: double distilled water, low dose group: PFOA 1 mg/( kg·d), middle dose group: PFOA 5 mg/( kg·d), high dose group: PFOA 25 mg/( kg·d), and were administrated by gavage once a day for 14 days take the organization after anesthesia, according to the follow-up experiments need treatment. The activity of oxidative stressrelated enzymes and the content of malondialdehyde( MDA) in liver tissue were detected. The mRNA levels of peroxisome proliferators-activited receptors α( PPARα) and cytochrome P4504A1( CYP4A1) were detected by real-time PCR. The protein expression of PPARα was detected by Western blot., Results: There was significant difference between high dose group and control group of the body weight( P < 0. 05). The liver weight and relative liver weight of the middle and high dose groups were significantly higher than those of the control group( P < 0. 05). The activity of superoxide dismutase( SOD) and glutathione peroxidase( GSH-Px) in the liver of the low dose group were significantly higher than that of the control group( P < 0. 05). The content of MDA in liver of middle and high dose groups were increased by 2. 5 times and 3. 5 times compared with that of control group( P < 0. 05). The expression of PPARα and its regulated CYP4A1 mRNA were significantly increased in low, middle and high dose groups. The expression of PPARα protein in the low, middle and high dose groups were up-regulated., Conclusion: PFOA exposure can lead to oxidative stress in rat liver, resulting in antioxidant enzymes SOD and GSH-Px and MDA changes. At the same time, PFOA exposure induced up regulation of PPARα and CYP4A1 in the liver of rats to enhance theβ-oxidation of fatty acids, leading to lipid peroxidation, which has obvious toxic effects on rat liver.