Effect of high fluoride and high fat on serum lipid levels and oxidative stress in rabbits

Sun, Lingyun; Gao, Yanhui; Zhang, Wei; Liu, Hui; Sun, Dianjun

doi:10.1016/j.etap.2014.10.010

Cited by 20 publications

(8 citation statements)

References 20 publications

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“…Total antioxidant capacity is considered to be the integrated action of all the antioxidants present in plasma and body fluids, thus providing an insight into a delicate balance in vivo between oxidants and antioxidants (Ghiselli et al, 2000). This is consistent with a report that high fat significantly elevated MDA levels and lowered T-AOC levels in the serum of rabbits (Sun et al, 2014). …”

Section: Discussionsupporting

confidence: 94%

Available energy content, nutrients digestibility of chili meal and effects on performance of growing pigs

Fan

Yang

et al. 2017

Animal Feed Science and Technology

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Section: Discussionsupporting

confidence: 94%

Available energy content, nutrients digestibility of chili meal and effects on performance of growing pigs

Fan

Yang

et al. 2017

Animal Feed Science and Technology

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“…Recently, several studies revealed the effects of F on lipid metabolism [ 31 – 35 ].To our knowledge, this is the first study to highlight the mechanisms by which F alters hepatic lipid metabolism depending on the time of exposure and the content of the diet. In addition, this response may be secondary to the well-known F-induced ER oxidative stress [ 3 , 15 , 17 , 34 – 37 ]. Conclusions based on our results can be inferred after observing a reduction in liver lipid droplets after treatment with F for 20 days in hypercaloric-fed rats.…”

Section: Discussionmentioning

confidence: 99%

Fluoride Intensifies Hypercaloric Diet-Induced ER Oxidative Stress and Alters Lipid Metabolism

et al. 2016

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The role of fluoride (F) in oxidative stress is well reported, but its effects on the lipid metabolism has not been completely exploredBackgroundHere, we evaluated the relationship of diet and F-induced oxidative stress to lipid metabolism in the liver of rats eating normocaloric or hypercaloric diets for two time periods (20 or 60 days).MethodsSeventy-two 21-day-old Wistar rats were divided into 2 groups (n = 36) based on the type of diet they were eating; each of these groups was then further divided into another two groups (n = 18) based on the time periods of either 20 or 60 days, for a total of four groups. Each of these was divided into 3 subgroups (n = 6 animals/subgroup), dependent on the dose of F administered in the drinking water (0 mg/L(control), 15 mg/L or 50 mg/L). After the experimental period, blood samples and the liver were collected. Plasma samples were analyzed for HDL, cholesterol and triglycerides. Western blots were performed to probe for GRP78, Erp29, SOD2, Apo-E and SREBP in hepatic tissues.ResultsAs expected,the expression of target proteins involved in oxidative stress increased in the F-treated groups, especially in liver tissue obtained from animals eating a hypercaloric diet. Most changes in the lipid levels and pathological conditions were seen earlier in the time period, at day 20. The morphometric analyses showed a reduction in steatosis in groups on ahypercaloric diet and treated with 50 mg F/L compared to the control, while no changes were obtained in normocaloric-fed rats. Accordingly, plasma TG was reduced in the F-treated group. The reduced expression of Apo-E in a time- and diet-dependent pattern may account for the particular decrease in steatosis in hypercaloric-fed F-treated rats.ConclusionsThese results suggest that F changes liver lipid homeostasis, possibly because of the induction of oxidative stress, which seems to be higher in animals fed hypercaloric diets.

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“…It is well-documented that oxidative stress plays an important role in the pathogenesis of endemic fluorosis [26][27][28]. Therefore, based on the data described above [25], we inferred that oxidative stress may be a modulator of fluoride-induced ET-1 over-expression.…”

Section: Discussionmentioning

confidence: 87%

“…This stiffness is closely related to oxidative stress [23,24]. In our previous study, we found that excess intake of fluoride via drinking water significantly increased lipid peroxidation and malondialdehyde levels and caused oxidative stress products to accumulate [25], indicating that oxidative stress caused by excess fluoride intake may play an important role in vascular stiffness observed in experimental animals.…”

Section: Discussionmentioning

confidence: 99%

Mechanisms Underlying Endothelin-1 Level Elevations Caused by Excessive Fluoride Exposure

Sun

Gao

Zhang³

et al. 2016

Cell Physiol Biochem

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Objective: To explore the mechanisms underlying endothelin-1 (ET-1) elevations induced by excessive fluoride exposure. Methods: We measured serum and bone fluoride ion content and plasma ET-1 levels and compared these parameters among different groups in an animal model. We also observed morphological changes in the aorta and endothelium of rabbits. In cell experiments, human umbilical vein endothelial cells (HUVECs) were treated with varying concentrations of NaF for 24h, with or without 10 µM U0126 pretreatment for 1 h. ET-1 levels in culture fluid and intracellular reactive oxygen species (ROS) levels, as well as ET1 gene, endothelin-converting enzyme-1 (ECE-1), extracellular signal-regulating kinase 1/2 (ERK1/2), pERK1/2 expression levels and RAS activation were measured and compared among the groups. Results: Plasma ET-1 levels of rabbits increased significantly in fluorinated groups compared with those in the control group. The rabbit thoracic aortas became slightly hardened in fluorinated groups compared with those in the control group, and some vacuoles were present in the endothelial cell cytoplasm of the rabbits in fluorinated groups. In our cell experiments, ET1 gene and ECE-1 expression levels in HUVECs and ET-1 expression levels in the cell culture supernatants increased significantly in some experimental groups compared with those in the control group. These trends paralleled the changes in intracellular ROS levels, RAS activation, and the pERK1/2-to-ERK1/2 ratio. After U0126 was added, ECE-1 expression and ET-1 levels decreased significantly. Conclusion: Excessive fluoride exposure leads to characteristic endothelial damage (vacuoles), thoracic aorta hardening, and plasma ET-1 level elevations in rabbits. In addition, the ROS-RAS-MEK1/2-pERK1/2/ERK1/2 pathway plays a crucial—and at least partial—role in ET-1 over-expression, which is promoted by excessive fluoride exposure.

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Effect of high fluoride and high fat on serum lipid levels and oxidative stress in rabbits

Cited by 20 publications

References 20 publications

Available energy content, nutrients digestibility of chili meal and effects on performance of growing pigs

Available energy content, nutrients digestibility of chili meal and effects on performance of growing pigs

Fluoride Intensifies Hypercaloric Diet-Induced ER Oxidative Stress and Alters Lipid Metabolism

Mechanisms Underlying Endothelin-1 Level Elevations Caused by Excessive Fluoride Exposure

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