Protective effect of sulforaphane against cisplatin-induced mitochondrial alterations and impairment in the activity of NAD(P)H: Quinone oxidoreductase 1 and γ glutamyl cysteine ligase: Studies in mitochondria isolated from rat kidney and in LLC-PK1 cells

Guerrero-Beltrán, Carlos Enrique; Calderón‐Oliver, Mariel; Martínez-Abundis, Eduardo; Tapia, Edilia; Zarco-Márquez, Guillermo; Zazueta, Cecilia; Pedraza‐Chaverrí, José

doi:10.1016/j.toxlet.2010.08.009

Cited by 53 publications

(37 citation statements)

References 39 publications

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“…CT control (vehicle). Data are presented as mean ± SEM, n = 4-6, *P \ 0.05 versus CT, # P \ 0.05 versus CP alterations characterized by decreased mitochondrial mass, disruption of cristae, and extensive mitochondrial swelling in proximal tubular epithelium [44], reduction of aconitase activity [27], reduction of antioxidant activity, and increase of oxidative damage [47] and ROS production [17].…”

Section: Discussionmentioning

confidence: 99%

“…Absorbance tracings were obtained and displayed in a double beam spectrophotometer at 525-575 nm. Mitochondrial calcium movement was analyzed by a similar assay but the absorbance tracings were determined at 675-685 nm using arsenazo III (60 lM) dye as indicator [27]. In both cases, the reaction was initiated by the addition of 100 lM Ca 2?…”

Section: Mitochondrial Membrane Potential (Dw) and Calcium Retentionmentioning

confidence: 99%

“…The activity of aconitase was assayed by determining the rate of formation of the intermediate product, cis-aconitate, from the interconversion of L-citrate and isocitrate at 240 nm [27]. Briefly, the reaction was carried out in 1 mL of reaction medium containing 25 mM KH 2 PO 4 ?…”

Section: Oxidative Stress Markersmentioning

confidence: 99%

“…In fact, mitochondria are both a target and an early event in CP-induced nephrotoxicity [19,24,25]. Several studies have shown the prevention of CP-induced mitochondrial dysfunction by the use of synthetic or natural antioxidants such as carvedilol [26], sulforaphane [27], and 5-aminolevulinic acid [28]. Based on the above information, the hypothesis was made that C-PC may prevent the CPinduced kidney mitochondrial alterations.…”

Section: Introductionmentioning

confidence: 99%

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C-phycocyanin prevents cisplatin-induced mitochondrial dysfunction and oxidative stress

et al. 2015

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The potential of C-phycocyanin (C-PC) to prevent cisplatin (CP)-induced kidney mitochondrial dysfunction was determined in CD-1 male mice. The CP-induced mitochondrial dysfunction was characterized by ultrastructural abnormalities and by decrease in the following parameters in isolated kidney mitochondria: adenosine diphosphate (ADP)-induced oxygen consumption (state 3), respiratory control ratio, ADP/oxygen (ADP/O) ratio, adenosine triphosphate synthesis, membrane potential, calcium retention, glutathione (GSH) content, and activity of respiratory complex I, aconitase, catalase, and GSH peroxidase. These mitochondria also showed increase in hydrogen peroxide production, malondialdehyde, and 3-nitrotyrosine protein adducts content. The above-described changes, as well as CP-induced nephrotoxicity, were attenuated in mice pretreated with a single injection of C-PC. Our data suggest that the attenuation of mitochondrial abnormalities is involved in the protective effect of C-PC against CP-induced nephrotoxicity. This is the first demonstration that C-PC pretreatment prevents CP-induced mitochondrial dysfunction in mice.

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Section: Discussionmentioning

confidence: 99%

Section: Mitochondrial Membrane Potential (Dw) and Calcium Retentionmentioning

confidence: 99%

Section: Oxidative Stress Markersmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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C-phycocyanin prevents cisplatin-induced mitochondrial dysfunction and oxidative stress

et al. 2015

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“…Antioxidants such as N-acetyl-cysteine (NAC) and SFN are often recommended to use in the clinic to re-establish the depleted levels of GSH and counteract drug-mediated oxidative stress McWalter et al 2004;Kang et al 2005;Fimognari et al 2008;Lu 2009;Moradi et al 2009;Guerrero-Beltran et al 2010;Chen et al 2010;Sevgiler and Uner 2010). NAC is a cysteine donor, which stimulates GSH synthesis.…”

Section: Potential Treatments Against Mdma-mediated Hepatotoxicitymentioning

confidence: 99%

A mechanistic insight into 3,4-methylenedioxymethamphetamine (“ecstasy”)-mediated hepatotoxicity

Antolino-Lobo

Meulenbelt

Berg

et al. 2011

Veterinary Quarterly

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3,4-Methylenedioxymethamphetamine (MDMA, ''ecstasy'') is a popular drug of abuse among young people with stimulant and hallucinogenic properties. The drug is generally thought to be safe among consumers due to its low-mortality rates. However, MDMA-adverse effects can occur and the risks are not clearly associated to a specific pattern since the consumption quantity seems not to be correlated with the initiation and severity of the injury. MDMA-mediated adverse health effects have been widely studied and can be evoked by multiple factors such as hyperthermia, polydrug abuse (drug-drug interactions), the altered release of neurotransmitters, impairment of mitochondrial function and apoptosis, metabolism and immune responses. Another adverse effect often associated with MDMA is liver toxicity, yet the mechanism of MDMA-induced liver toxicity is not completely understood. A critical starting point appears to be the hepatic metabolism of MDMA by phase I and II enzymes, leading to reactive metabolites. Elucidating the mechanism of hepatic injury mediated by MDMA is of high toxicological and clinical relevance. In this review, an overview of the literature and the latest findings with respect to the mechanism of MDMA-mediated liver toxicity is described.

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Sulforaphane and ophthalmic diseases

Zhang,

Zhao,

Liu

et al. 2024

Food Science & Nutrition

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Sulforaphane (SFN) is an organosulfur compound categorized as an isothiocyanate (ITC), primarily extracted from cruciferous vegetables like broccoli and cabbage. The molecular formula of sulforaphane (SFN) is C6H11NOS2. SFN is generated by the hydrolysis of glucoraphanin (GRP) through the enzyme myrosinase, showing notable properties including anti‐diabetic, anti‐inflammatory, antimicrobial, anti‐angiogenic, and anticancer attributes. Ongoing clinical trials are investigating its potential in diseases such as cancer, neurodegenerative diseases, diabetes‐related complications, chronic kidney disease, cardiovascular disease, and liver diseases. Several animal carcinogenesis models and cell culture models have shown it to be a very effective chemopreventive agent, and the protective effects of SFN in ophthalmic diseases have been linked to multiple mechanisms. In murine models of diabetic retinopathy and age‐related macular degeneration, SFN delays retinal photoreceptor cell degeneration through the Nrf2 antioxidative pathway, NF‐κB pathway, AMPK pathway, and Txnip/mTOR pathway. In rabbit models of keratoconus and cataract, SFN has been shown to protect corneal and lens epithelial cells from oxidative stress injury by activating the Keap1‐Nrf2‐ARE pathway and the Nrf‐2/HO‐1 antioxidant pathway. Oral delivery or intraperitoneal injection at varying concentrations are the primary strategies for SFN intake in current preclinical studies. Challenges remain in the application of SFN in eye disorders due to its weak solubility in water and limited bioavailability because of the presence of blood–ocular barrier systems. This review comprehensively outlines recent research on SFN, elucidates its mechanisms of action, and discusses potential therapeutic benefits for eye disorders such as age‐related macular degeneration (AMD), diabetic retinopathy (DR), cataracts, and other ophthalmic diseases, while also indicating directions for future clinical research to achieve efficient SFN treatment for ophthalmic diseases.

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Protective effect of sulforaphane against cisplatin-induced mitochondrial alterations and impairment in the activity of NAD(P)H: Quinone oxidoreductase 1 and γ glutamyl cysteine ligase: Studies in mitochondria isolated from rat kidney and in LLC-PK1 cells

Cited by 53 publications

References 39 publications

C-phycocyanin prevents cisplatin-induced mitochondrial dysfunction and oxidative stress

C-phycocyanin prevents cisplatin-induced mitochondrial dysfunction and oxidative stress

A mechanistic insight into 3,4-methylenedioxymethamphetamine (“ecstasy”)-mediated hepatotoxicity

Sulforaphane and ophthalmic diseases

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