Suppressive Effect of Superoxide Dismutase on Adriamycin Nephropathy

Okasora, Teruo; Takikawa, Takako; Utsunomiya, Yasushi; Senoh, Isonori; Hayashibara, Hiroshi; Shiraki, Kazuo; Kasagi, Tsunakiyo; Shimizu, Fujio

doi:10.1159/000186739

Cited by 69 publications

(59 citation statements)

References 9 publications

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“…In another study performed on Wistar rats, SOD activity has been significantly decreased in B(a)P treated group [25]. It has been also reported that 7.5 mg/kg doxorubicin induces superoxide dismutase [14]. In our study, SOD activity and MDA increased while CAT activity decreased following a long-term B(a)P treatment, and SOD activity slightly decreased in 4 mg/kg doxorubicin treated group.…”

Section: Discussionsupporting

confidence: 71%

“…Doxorubicin is bound to sugar-phosphate structure by cross-linking the DNA after penetrating into close base pairs of the DNA chain in rapidly reproducing cancerous cells. It damages the DNA structure and consequently the RNA synthesis [14,15]. Excretion of doxorubicin occurs predominantly by the hepatobiliary route and partially by the kidneys.…”

Section: Introductionmentioning

confidence: 99%

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The effect of doxorubicin on rats that received toxic and carcinogenic benzo(a)pyrene.

Coşan

Başaran²,

Güneş³

et al. 2008

Folia Histochem Cytobiol.

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Section: Discussionsupporting

confidence: 71%

Section: Introductionmentioning

confidence: 99%

The effect of doxorubicin on rats that received toxic and carcinogenic benzo(a)pyrene.

Coşan

Başaran²,

Güneş³

et al. 2008

Folia Histochem Cytobiol.

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“…26,27 It was also suggested that ADR-mediated ROS markedly increase the peroxidation of membrane polyunsaturated phospholipids and this lipid peroxidation level in vivo may be involved in the nephrotoxicity of ADR. 28 At the end of the treatment period of drug, we observed that the ADR treatment significantly reduced the MMP and slightly ATP level.…”

Section: Discussionmentioning

confidence: 99%

The restoration of kidney mitochondria function by inhibition of angiotensin-II production in rats with acute adriamycin-induced nephrotoxicity

et al. 2014

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Adriamycin (ADR) is commonly used for many solid tumor treatments. Its clinical utility is, however, largely limited by the adverse reactions, are known to be nephrotoxic. The mechanism by which it induces kidney damage is still not completely understood, but its nephrotoxicity might relate to increase reactive oxidant status (ROS), mitochondrial dysfunction. Until now, neurohormonal activation of it is unclear. ADR might activate the renin angiotensin system. Angiotensin-II also induced ROS and mitochondrial dysfunction. The aim of this study was to investigate whether angiotensin-II production inhibition has the protective effect on attenuation of mitochondrial function in rats with acute ADR-nephrotoxicity or not. Rats were divided into five groups as a control, ADR, co-treated ADR with captopril (CAP), co-treated ADR with Aliskren, co-treated ADR with both CAP and Aliskren groups. Creatinine kinase (CK) levels were measured at the end of treatment period. The kidneys were homogenized and biochemical measurements were made in mitochondria, cytosol. Mitochondria membrane potential (MMP) and ATP levels were determined. ADR increased CK levels and oxidative stress in mitochondria too (p50.05). ADR significantly decreased MMP and ATP level in kidney mitochondria (p50.05). Co-administration with ADR and Aliskren and CAP improved the dissipation of MMP (p50.05). The decrease in ATP level was restored by treatment with inhibitors of ACE and renin. We concluded that inhibitors of angiotensin-II are effective against acute ADR induced nephrotoxicity via the restoration of MMP and ATP production and prevention of mitochondrial damage in vivo. KeywordsAdriamycin-induced nephrotoxicity, Aliskren, captopril, mitochondrial ATP, mitochondrial membrane potential, oxidative stress index History

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“…Indeed, adriamycin-, puromycin-, or cisplatin-induced nephrotic syndrome has been reported to be exacerbated by reactive oxygen species. [15][16][17][18][19][20] In addition, studies have reported that the antioxidant vitamin E and the antihypercholesterolemic agent probucol reduce nephrotoxicity. 21,22) However, few drugs with antioxidant activity are clinically available, and such drugs are not used for antioxidant purposes.…”

Section: Discussionmentioning

confidence: 99%

The Effect of Eriobotrya japonica Seed Extract on Oxidative Stress in Adriamycin-Induced Nephropathy in Rats

Hamada

Yoshioka

Takuma

et al. 2004

Biological & Pharmaceutical Bulletin

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Recent studies have shown that oxidative damage in the body induced by reactive oxygen species (ROS) and free radicals is frequently involved in the development of many diseases.1-3) ROS are continuously produced physiologically, and play an important role in the expression of cell functions such as the transmission of impulse information. However, if they are produced excessively from any cause, they act cytotoxically as mediators of adverse events such as inflammation, necrosis, and apoptosis. In the kidney, ROS are important causes of acute and subacute renal failure in most cases. It has also been reported that renal failure results from decreased levels of the antioxidant vitamin E and decreased activity of the antioxidant enzyme glutathione peroxidase (GPx), 4,5) and can be prevented by free-radical scavengers and polyphenols. 6,7) Also, certain anticancer drugs themselves produce free radicals, and act as factors promoting nephrotoxicity. 8) In particular, adriamycin (ADR), which is used to treat leukemia and lung cancer, generates superoxide anions and hydroxy radicals, thereby inducing nephrotoxicity, suggesting that the administration of antioxidant substances is effective in inhibiting nephrotoxicity. However, no clinically useful drugs are currently available.Eriobotrya japonica is widely cultivated as a fruit crop. Among Chinese medicine preparations, Eriobotrya japonica folia are an ingredient in Shini-seihai-to and Biwayo-to used as antiphlogistic, analgesic, antitussive, and expectorant agents. Recently, the blood sugar-reducing 9-11) and antiphlogistic actions 12,13) of Eriobotrya japonica folia have also been reported. On the other hand, Eriobotrya japonica seeds, like those of apricots and peaches of the same genus (Rosaceae), contain amygdalin as the main constituent; therefore, they were used as a substitute medication for the latter seeds in prewar Japan.To date, we have discovered the antioxidant action and associated hepatotoxicity-inhibiting action of an extract from Eriobotrya japonica seeds.14) In this study, to clarify the physiological action of an extract from Eriobotrya japonica seeds, we administered an Eriobotrya japonica seed extract (ESE) with 70% ethanol to rats with ADR nephrotoxicity, and evaluated its improvement effect. MATERIALS AND METHODS MaterialsSufficiently sun-dried seeds of Mogi-loquant collected at Muroto and Susaki cities in Kochi Prefecture of Japan were the Eriobotrya japonica seeds used. Adriamycin (ADR) was provided by Kyowahakko (Japan). All other chemicals were of reagent grade.Extraction of Seed Eriobotrya japonica seeds were extracted by 70% ethanol. Briefly, 1.0 kg of seeds was crushed in a blender equipped with a refrigerator at 1000 rpm, and then continuously stirred by a mixer at 300 rpm for 7 d after being dissolved in the 70% ethanol. The supernatant was then collected and evaporated to dryness to prepare the dried extracts.Animals Male Wistar rats, aged seven weeks, 180-200 g, were purchased from NSC Japan. Animals were acclimatized for seven days ...

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Suppressive Effect of Superoxide Dismutase on Adriamycin Nephropathy

Cited by 69 publications

References 9 publications

The effect of doxorubicin on rats that received toxic and carcinogenic benzo(a)pyrene.

The effect of doxorubicin on rats that received toxic and carcinogenic benzo(a)pyrene.

The restoration of kidney mitochondria function by inhibition of angiotensin-II production in rats with acute adriamycin-induced nephrotoxicity

The Effect of Eriobotrya japonica Seed Extract on Oxidative Stress in Adriamycin-Induced Nephropathy in Rats

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