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Ascorbate-induced free radical toxicity to isolated islet cells
1Department of Clinical Chemistry, Umeå University, Sweden.
Summary
Vitamin C (ascorbate) can harm isolated mouse islet cells by generating free radicals. This cytotoxicity is linked to metal-catalyzed reactions, suggesting a potential role in diabetes development.
Area of Science:
- Biochemistry
- Cell Biology
- Endocrinology
Background:
- Ascorbate (Vitamin C) is known for generating cytotoxic free oxygen radicals.
- This property is shared with alloxan, a known diabetogenic drug.
- Previous reports suggest ascorbate may also possess diabetogenic properties.
Purpose of the Study:
- To investigate the cytotoxic effects of ascorbate on isolated mouse islet cells.
- To elucidate the mechanism underlying ascorbate-induced islet cell damage.
Main Methods:
- Isolated mouse islet cells were exposed to varying concentrations of ascorbate (0.5-2.0 mmol/l).
- Cell membrane permeability was assessed using trypan blue uptake.
- The role of free radicals was examined by testing the effects of antioxidants like superoxide dismutase and catalase, and metal chelators like DTPA.
Main Results:
- Ascorbate induced a concentration-dependent increase in trypan blue uptake, indicating increased cell membrane permeability.
- This cytotoxic effect was significantly inhibited by superoxide dismutase, catalase, cytochrome-c, and diethylenetriaminepentacetic acid (DTPA).
- D-mannitol did not inhibit the trypan blue uptake, suggesting the damage is not solely due to osmotic effects.
Conclusions:
- Ascorbate exhibits cytotoxicity towards isolated mouse islet cells.
- The mechanism involves the generation of free radicals, likely through metal-catalyzed reactions.
- These findings support the hypothesis that ascorbate could be diabetogenic.