Dose-Dependent Protection by Lipoic Acid against Cisplatin-Induced Nephrotoxicity in Rats: Antioxidant Defense System

Somani, Satu M.; Husain, Kazim; Whitworth, Craig; Trammell, Gary L.; Malafa, Mokenge P.; Rybak, Leonard P.

doi:10.1034/j.1600-0773.2000.d01-41.x

Cited by 134 publications

(54 citation statements)

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“…Oxidative damage and inflammatory events might explain the effects on other cellular constituents and have been associated with cisplatin-induced nephrotoxicity (Cvitkovic 1998;Ali and Al Moundhri 2006;Yao et al 2007;Pabla and Dong 2008). Several lines of evidence indicate that cisplatin nephrotoxicity is mainly associated with mitochondria-generated oxygen reactive species (ROS) (Matsushima et al 1998;Somani et al 2000;Chang et al 2002;Wang and Lippard 2005;Santos et al 2007;Santos et al 2008). Alterations in renal hemodynamic modulators have also been associated with the toxic effects of cisplatin on kidneys (Hye Khan et al 2007).…”

Section: The Antitumor Mechanism Versus the Nephrotoxic Mechanismmentioning

confidence: 97%

Cisplatin-induced nephrotoxicity and targets of nephroprotection: an update

et al. 2012

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Section: The Antitumor Mechanism Versus the Nephrotoxic Mechanismmentioning

confidence: 97%

Cisplatin-induced nephrotoxicity and targets of nephroprotection: an update

et al. 2012

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“…In various models, three agents, ␣-tocopherol, ascorbic acid, and ␣-lipoic acid, have been shown to reduce one or more types of oxidative stress (25)(26)(27)(28)(29)(30). Previous work has suggested that these agents may have additive effects when used together (31).…”

Section: Discussionmentioning

confidence: 99%

“…Mice were treated in accordance with the recommendations of the Association for Research in Vision and Ophthalmology. Litters of homozygous rd1͞rd1 mice in a C57BL͞6 background were given daily injections of a mixture of antioxidants (25)(26)(27)(28)(29)(30) including ␣-tocopherol (200 mg͞kg in olive oil), ascorbic . Daily injections of ␣-tocopherol or ␣-lipoic acid between P18 and P35 promote cone survival in rd1 mice.…”

Section: Methodsmentioning

confidence: 99%

Antioxidants reduce cone cell death in a model of retinitis pigmentosa

Komeima

Rogers

Lü³

et al. 2006

Proc. Natl. Acad. Sci. U.S.A.

375

367

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Retinitis pigmentosa (RP) is a label for a group of diseases caused by a large number of mutations that result in rod photoreceptor cell death followed by gradual death of cones. The mechanism of cone cell death is uncertain. Rods are a major source of oxygen utilization in the retina and, after rods die, the level of oxygen in the outer retina is increased. In this study, we used the rd1 mouse model of RP to test the hypothesis that cones die from oxidative damage. A mixture of antioxidants was selected to try to maximize protection against oxidative damage achievable by exogenous supplements; ␣-tocopherol (200 mg͞kg), ascorbic acid (250 mg͞kg), Mn(III)tetrakis (4-benzoic acid) porphyrin (10 mg͞kg), and ␣-lipoic acid (100 mg͞kg). Mice were treated with daily injections of the mixture or each component alone between postnatal day (P)18 and P35. Between P18 and P35, there was an increase in two biomarkers of oxidative damage, carbonyl adducts measured by ELISA and immunohistochemical staining for acrolein, in the retinas of rd1 mice. The staining for acrolein in remaining cones at P35 was eliminated in antioxidant-treated rd1 mice, confirming that the treatment markedly reduced oxidative damage in cones; this was accompanied by a 2-fold increase in cone cell density and a 50% increase in medium-wavelength cone opsin mRNA. Antioxidants also caused some preservation of cone function based upon photopic electroretinograms. These data support the hypothesis that gradual cone cell death after rod cell death in RP is due to oxidative damage, and that antioxidant therapy may provide benefit. oxidative damage ͉ photoreceptors ͉ retinal degenerations R etinitis pigmentosa (RP) refers to a group of diseases in which a mutation results in death of rod photoreceptors followed by gradual death of cones. The diseases referred to as RP show a similar phenotype consisting of pigmented spots scattered throughout the retina, narrowed retinal vessels, and retinal sheen suggesting atrophy. At one time, it was felt that inflammation was important in the pathogenesis, and hence the term ''retinitis'' was paired with a descriptor for the most prominent feature of the phenotype, the scattered pigment, resulting in the term retinitis pigmentosa. It is now known that this phenotype results whenever there is widespread rod photoreceptor cell death. Although toxins or infections can occasionally cause widespread rod death, it occurs most commonly when there is a mutation in a gene that is selectively expressed in rods and, either through gain or loss of function, the mutation promotes rod cell death. Mutations in 36 different genes have been found to cause RP, and mutations in many more cause widespread rod cell death in association with syndromes that have extraocular manifestations (www.sph.uth.tmc.edu͞RetNet͞ sum-dis.htm).How does diffuse death of rods throughout the retina result in the distinctive phenotype that ophthalmologists recognize as RP? Rods have an intimate relationship, both structurally and functionally, with retinal pigmen...

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“…Oxidative stress has been also implicated in cisplatin-induced nephrotoxicity. Cisplatin treatment increases renal lipid peroxidation, blood urea nitrogen, creatinine, and oxidized glutathione levels, but depletes renal glutathione (17)(18)(19). Large bolus of intravenous glutathione blocks these effects and cisplatin-induced nephrotoxicity (10).…”

mentioning

confidence: 99%