ArticleToxicology letters2012
Effect of garlic-derived organosulfur compounds on mitochondrial function and integrity in isolated mouse liver mitochondria.
Article in Toxicology letters, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 68 citations in OpenAlex.
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- Induction of Cyp2e1 contributes to asparaginase-induced hepatocyte sensitization to lipotoxicity.Acta pharmaceutica Sinica. B · 2025Article
- Unraveling the neuroprotective mechanisms of elephant black garlic extract against beta amyloid peptide-induced neurotoxicity.Frontiers in nutrition · 2025Article
- Aged garlic therapeutic intervention targeting inflammatory pathways in pathogenesis of bowel disorders.Heliyon · 2024Article
- Taurine Improves Sperm Mitochondrial Indices, Blunts Oxidative Stress Parameters, and Enhances Steroidogenesis and Kinematics of Sperm in Lead-Exposed Mice.Reproductive sciences (Thousand Oaks, Calif.) · 2023Article
- Advances of HAntioxidants (Basel, Switzerland) · 2023Review
- A comparative study of smart nanoformulations of diethyldithiocarbamate with CuScientific reports · 2023Article
- Diallyl trisulfide plays an antifibrotic role by inhibiting the expression of Bcl-2 in hepatic stellate cells.Journal of biochemical and molecular toxicology · 2022Article
- The crucial role of oxidative stress in non-alcoholic fatty liver disease-induced male reproductive toxicity: the ameliorative effects of Iranian indigenous probiotics.Naunyn-Schmiedeberg's archives of pharmacology · 2022Article
- Metformin alleviates cholestasis-associated nephropathy through regulating oxidative stress and mitochondrial function.Liver research (Beijing, China) · 2021Article
- Silymarin mitigates bile duct obstruction-induced cholemic nephropathy.Naunyn-Schmiedeberg's archives of pharmacology · 2021Article
- In Vitro and In Vivo Evidence on the Role of Mitochondrial Impairment as a Mechanism of Lithium-Induced Nephrotoxicity.Biological trace element research · 2021Article
- Taurine mitigates bile duct obstruction-associated cholemic nephropathy: effect on oxidative stress and mitochondrial parameters.Clinical and experimental hepatology · 2021Article
- Intranasal insulin improves mitochondrial function and attenuates motor deficits in a rat 6-OHDA model of Parkinson's disease.CNS neuroscience & therapeutics · 2021Article
- Mitochondrial dysfunction and oxidative stress are involved in the mechanism of tramadol-induced renal injury.Current research in pharmacology and drug discovery · 2021Article
- The Role of Mitochondrial Impairment and Oxidative Stress in the Pathogenesis of Lithium-Induced Reproductive Toxicity in Male Mice.Frontiers in veterinary science · 2021Article
- Taurine mitigates cirrhosis-associated heart injury through mitochondrial-dependent and antioxidative mechanisms.Clinical and experimental hepatology · 2020Article
- N-acetyl cysteine treatment preserves mitochondrial indices of functionality in the brain of hyperammonemic mice.Clinical and experimental hepatology · 2020Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
The objectives of this work were to evaluate the direct effects of diallysulfide (DAS) and diallyldisulfide (DADS), two major organosulfur compounds of garlic oil, on mitochondrial function and integrity, by using isolated mouse liver mitochondria in a cell-free system. DADS produced concentration-dependent mitochondrial swelling over the range 125-1000μM, while DAS was ineffective. Swelling experiments performed with de-energized or energized mitochondria showed similar maximal swelling amplitudes. Cyclosporin A (1μM), or ethylene glycol-bis(2-aminoethylether)-N,N,N',N'-tetraacetic acid (EGTA, 1mM) were ineffective in inhibiting DADS-induced mitochondrial swelling. DADS produced a minor (12%) decrease in mitochondrial membrane protein thiols, but did not induce clustering of mitochondrial membrane proteins. Incubation of mitochondria with DADS (but not DAS) produced an increase in the oxidation rate of 2',7' dichlorofluorescein diacetate (DCFH-DA), together with depletion of reduced glutathione (GSH) and increased lipid peroxidation. DADS (but not DAS) produced a concentration-dependent dissipation of the mitochondrial membrane potential, but did not induce cytochrome c release. DADS-dependent effects, including mitochondrial swelling, DCFH-DA oxidation, lipid peroxidation and loss of mitochondrial membrane potential, were inhibited by antioxidants and iron chelators. These results suggest that DADS causes direct impairment of mitochondrial function as the result of oxidation of the membrane lipid phase initiated by the GSH- and iron-dependent generation of oxidants.
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