2004Unpublished venueRequires access

ANTAGONISTIC EFFECT OF SELENIUM ON OXIDATIVE STRESS, DNA DAMAGE, AND APOPTOSIS INDUCED BY FLUORIDE IN HUMAN HEPATOCYTES

Aiguo Wang, Tao Xia, Rian Ru, Jing Yuan, Xuemin Chen, Kedi Yang

Open publisher page 33 citations

Abstract

SUMMARY: To evaluate the toxicity of fluoride and the antagonistic effect of selenium, normal human primary hepatocytes were incubated with sodium fluoride (80 µg/mL) and/or sodium selenite (1.73 µg/mL) for 12 hr in vitro. The percentage of apoptotic hepatocytes, the number of cells in S phase, DNA damage in cells, and lipid peroxide (LPO) levels in the cells and culture medium, together with aspartate transaminase (AST) and lactate dehydrogenase (LDH) activities in the cell culture medium, were higher in the fluoride-exposed group than in the control group, but the glutathione (GSH) content in the fluorideexposed cells was lower than in the control group. However, these toxic effects of fluoride were reduced by selenium, which elevated the GSH content and reduced the LPO levels, the LDH and AST activities, and the percentage of apoptotic and DNA-damaged cells. These findings suggest that fluoride exposure can cause hepatocyte damage, whereas selenium can antagonize fluoride-induced apoptosis, DNA damage, and oxidative stress in hepatocytes.

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SUMMARY: To evaluate the toxicity of fluoride and the antagonistic effect of selenium, normal human primary hepatocytes were incubated with sodium fluoride (80 µg/mL) and/or sodium selenite (1.73 µg/mL) for 12 hr in vitro. The percentage of apoptotic hepatocytes, the number of cells in S phase, DNA damage in cells, and lipid peroxide (LPO) levels in the cells and culture medium, together with aspartate transaminase (AST) and lactate dehydrogenase (LDH) activities in the cell culture medium, were higher in the fluoride-exposed group than in the control group, but the glutathione (GSH) content in the fluorideexposed cells was lower than in the control group. However, these toxic effects of fluoride were reduced by selenium, which elevated the GSH content and reduced the LPO levels, the LDH and AST activities, and the percentage of apoptotic and DNA-damaged cells. These findings suggest that fluoride exposure can cause hepatocyte damage, whereas selenium can antagonize fluoride-induced apoptosis, DNA damage, and oxidative stress in hepatocytes.

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Available abstract

SUMMARY: To evaluate the toxicity of fluoride and the antagonistic effect of selenium, normal human primary hepatocytes were incubated with sodium fluoride (80 µg/mL) and/or sodium selenite (1.73 µg/mL) for 12 hr in vitro. The percentage of apoptotic hepatocytes, the number of cells in S phase, DNA damage in cells, and lipid peroxide (LPO) levels in the cells and culture medium, together with aspartate transaminase (AST) and lactate dehydrogenase (LDH) activities in the cell culture medium, were higher in the fluoride-exposed group than in the control group, but the glutathione (GSH) content in the fluorideexposed cells was lower than in the control group. However, these toxic effects of fluoride were reduced by selenium, which elevated the GSH content and reduced the LPO levels, the LDH and AST activities, and the percentage of apoptotic and DNA-damaged cells. These findings suggest that fluoride exposure can cause hepatocyte damage, whereas selenium can antagonize fluoride-induced apoptosis, DNA damage, and oxidative stress in hepatocytes.

Key concepts: Fluoride, Sodium fluoride, Oxidative stress, Glutathione, Selenium, Apoptosis, Chemistry, Lactate dehydrogenase

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ANTAGONISTIC EFFECT OF SELENIUM ON OXIDATIVE STRESS, DNA DAMAGE, AND APOPTOSIS INDUCED BY FLUORIDE IN HUMAN HEPATOCYTES — Research Paper | ScholarLens