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Mitochondrial dysfunction in an animal model of hyperoxaluria: a prophylactic approach with fucoidan
Coothan Kandaswamy Veena1, Anthony Josephine, Sreenivasan P Preetha
1Department of Medical Biochemistry, Dr. ALM. Post Graduate Institute of Basic Medical Sciences, University of Madras, Taramani Campus, Chennai - 600 113, India.
Abstract:
Oxalate/calcium oxalate toxicity is mediated through generation of reactive oxygen species in a process that partly depends upon events that induce mitochondrial damage. Mitochondrial dysfunction is an important event favoring stone formation. The objective of the present study was to investigate whether mitochondria is a target for oxalate/calcium oxalate and the plausible role of naturally occurring glycosaminoglycans from edible seaweed, fucoidan in ameliorating mitochondrial damage. Male albino rats of Wistar strain were divided into four groups and treated as follows: Group I: vehicle treated control, Group II: hyperoxaluria was induced with 0.75% ethylene glycol in drinking water for 28 days, Group III: fucoidan from F. vesiculosus (5 mg/kg b.wt, s.c) from the 8th day of the experimental period, Group IV: ethylene glycol+fucoidan treated rats. The tricarboxylic acid (TCA) cycle enzymes like succinate dehydrogenase, isocitrate dehydrogenase, malate dehydrogenase and respiratory complex enzyme activities were assessed to evaluate mitochondrial function. Oxidative stress was assessed based on the activities of antioxidant enzymes, level of reactive oxygen species, lipid peroxidation and reduced glutathione. Mitochondrial swelling was also analyzed. Ultra structural changes in renal tissue were analyzed with electron microscope. Hyperoxaluria induced a decrease in the activities of TCA cycle enzymes and respiratory complex enzymes. The oxidative stress was evident by the decrease in antioxidant enzymes, glutathione and an increase in reactive species and lipid peroxidation in mitochondria. Mitochondrial damage was evident by increased mitochondrial swelling. Administration of fucoidan, decreased reactive oxygen species, lipid peroxidation (P<0.05), mitochondrial swelling and increased the activities of antioxidant enzymes and glutathione levels (P<0.05) and normalized the activities of mitochondrial TCA cycle and respiratory complex enzymes (P<0.05). From the present study, it can be concluded that mitochondrial damage is an essential event in hyperoxaluria, and fucoidan was able to effectively prevent it and thereby the renal damage in hyperoxaluria.
Insights
Oxalate causes kidney damage by inducing mitochondrial dysfunction. Fucoidan, a seaweed extract, effectively protects mitochondria from this damage, preventing kidney injury in hyperoxaluric rats.
Area of Science:
- Biochemistry
- Nephrology
- Pharmacology
Background:
- Oxalate and calcium oxalate contribute to kidney stone formation by inducing oxidative stress and mitochondrial damage.
- Mitochondrial dysfunction is a key factor in the pathogenesis of hyperoxaluria-induced renal damage.
Purpose of the Study:
- To investigate if mitochondria are a target of oxalate/calcium oxalate toxicity.
- To evaluate the protective role of fucoidan, a seaweed-derived glycosaminoglycan, against oxalate-induced mitochondrial damage.
Main Methods:
- Hyperoxaluric male albino rats were induced using ethylene glycol and treated with or without fucoidan.
- Mitochondrial function was assessed by measuring tricarboxylic acid (TCA) cycle and respiratory complex enzyme activities.
- Oxidative stress markers, including reactive oxygen species (ROS), lipid peroxidation, and glutathione levels, were analyzed.
- Mitochondrial swelling and ultrastructural changes in renal tissue were examined.
Main Results:
- Ethylene glycol-induced hyperoxaluric rats exhibited decreased TCA cycle and respiratory enzyme activities, increased oxidative stress, and significant mitochondrial swelling.
- Fucoidan administration significantly reduced ROS and lipid peroxidation, increased antioxidant enzyme and glutathione levels, and ameliorated mitochondrial swelling.
- Fucoidan treatment normalized the activities of mitochondrial TCA cycle and respiratory complex enzymes, indicating restored mitochondrial function.
Conclusions:
- Mitochondrial damage is a critical event in hyperoxaluric kidney injury.
- Fucoidan effectively mitigates oxalate-induced mitochondrial damage and subsequent renal injury by reducing oxidative stress and restoring mitochondrial function.
