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4,4'-Dichloro-diphenyl diselenide modulated oxidative stress that differently affected peripheral tissues in
Luiza S Marques1, Vanessa A Zborowski1, Suélen O Heck1
1Laboratory of Synthesis, Reactivity, Pharmacological and Toxicological Evaluation of Organochalcogens, Department of Biochemistry and Molecular Biology, Center of Natural and Exact Sciences, Federal University of Santa Maria, Santa Maria, RS 97105-900, Brazil.
Abstract:
Streptozotocin (STZ) is a substance used experimentally to induce a diabetes model, a metabolic disease associated with oxidative tissue damage. This study evaluated if 4-4'-dichloro-diphenyl diselenide (p-ClPhSe)2 modulates oxidative stress in peripheral tissues of diabetic mice. Male Swiss mice received a single STZ injection (i.p.) at a dose of 200 mg/kg or its vehicle and were treated with (p-ClPhSe)2 (7 days, 5 mg/kg) or metformin (200 mg/kg, twice per day). After, the mice were euthanized to collect liver, kidney, and skeletal muscle samples. In the liver, (p-ClPhSe)2 reduced thiobarbituric acid reactive substances (TBARS) and protein carbonyl levels and normalized the superoxide dismutase activity in STZ-treated mice. In the kidney, (p-ClPhSe)2 reversed the increase in the reactive species levels but not the catalase (CAT) activity reduction in STZ-treated mice. There was no evidence of oxidative damage in the skeletal muscle of STZ-treated mice, but an increase in the CAT activity and a reduction in non-protein thiol levels were found. (p-ClPhSe)2 did not reverse a decrease in hepatic and renal δ-aminolevulinic acid dehydratase activity in STZ-treated mice. The results show that the liver and kidney of STZ-treated mice were more susceptible to oxidative stress. This study reveals that (p-ClPhSe)2 modulated oxidative stress, which differently affected peripheral tissues of diabetic mice.
Insights
This study shows that 4-4'-dichloro-diphenyl diselenide, a novel compound, can reduce oxidative stress in the liver and kidney of diabetic mice. It offers potential therapeutic benefits for managing diabetes-related tissue damage.
Area of Science:
- Biochemistry
- Pharmacology
- Toxicology
Background:
- Streptozotocin (STZ) induces a diabetes model in mice, characterized by oxidative tissue damage.
- Oxidative stress is a key factor in the pathogenesis of diabetes and its complications.
- Peripheral tissues like the liver, kidney, and skeletal muscle are affected by diabetes-induced oxidative stress.
Purpose of the Study:
- To evaluate the potential of 4-4 '-dichloro-diphenyl diselenide ((p-ClPhSe)2) to modulate oxidative stress in peripheral tissues of STZ-induced diabetic mice.
- To compare the effects of (p-ClPhSe)2 with metformin, a standard antidiabetic drug, in managing oxidative stress.
- To investigate the impact of (p-ClPhSe)2 on specific biomarkers of oxidative damage and antioxidant activity in different tissues.
Main Methods:
- Male Swiss mice were injected with streptozotocin (STZ) to induce diabetes.
- Diabetic mice were treated with either (p-ClPhSe)2 (5 mg/kg) or metformin (200 mg/kg).
- Liver, kidney, and skeletal muscle tissues were collected to assess thiobarbituric acid reactive substances (TBARS), protein carbonyls, superoxide dismutase (SOD), catalase (CAT) activity, and non-protein thiol levels.
Main Results:
- In the liver, (p-ClPhSe)2 significantly reduced TBARS and protein carbonyl levels and normalized SOD activity in STZ-treated mice.
- In the kidney, (p-ClPhSe)2 reversed the increase in reactive species levels but did not restore CAT activity.
- Skeletal muscle showed no oxidative damage, but exhibited increased CAT activity and reduced non-protein thiols; (p-ClPhSe)2 did not reverse these changes. Hepatic and renal δ-aminolevulinic acid dehydratase activity was not restored by (p-ClPhSe)2.
Conclusions:
- The liver and kidney are more susceptible to STZ-induced oxidative stress than skeletal muscle.
- (p-ClPhSe)2 demonstrates a capacity to modulate oxidative stress in peripheral tissues of diabetic mice, particularly in the liver and kidney.
- The findings suggest that (p-ClPhSe)2 may hold therapeutic potential for managing diabetes-related oxidative damage, with differential effects across tissues.
