Changes in lipid peroxidation and activities of xanthine oxidase, superoxide dismutase and catalase in kidneys of cephaloridine-administered rats.

Suzuki, Yoshihiro; Sudo, Jun-ichi

doi:10.1254/jjp.49.43

Cited by 10 publications

(4 citation statements)

References 30 publications

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“…In the physiological study, however, proteinuria and the increases of S-CRE and S-UN occurred, suggesting damage to the glomeru lus. It is known that CER generates superoxide anions in the renal cells (20). Thus, these oxygen radicals might have induced the peroxidation of the cellular membrane at the glomerulus, resulting in the functional damage of the glomerulus (25).…”

Section: Discussionmentioning

confidence: 99%

“…As indexes of renal failure, serum creatinine (S-CRE) and urea nitro gen (S-UN) were measured with an autoanalyzer (AU510; Olympus, Tokyo). It is reported that both S-UN and uri nary glucose (U-GLU) begin to rise at the 1st day, reach ing the maximal level on the 3rd day, with the values being 10 times higher than the control level, and are still higher until the 7th day compared with the normal level (20). Based on this previous observation, the period for this experiment was set up.…”

Section: Cer-induced Arfmentioning

confidence: 99%

“…CER-induced ARF was produced according to the previous method (20). In brief, the rats were divided into 6 groups: the normal group (5 rats) and 5 groups of CER induced ARF (12 rats in each group).…”

Section: Cer-induced Arfmentioning

confidence: 99%

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Effects of KW-3902, a Novel Adenosine A1-Receptor Antagonist, on Cephaloridine-Induced Acute Renal Failure in Rats

Nagashima

Kusaka

Satô

et al. 1994

Japanese Journal of Pharmacology

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ABSTRACT-We investigated the possible renal protective effects of -1,3 dipropylxanthine), a selective and potent adenosine A,-receptor antagonist, against cephaloridine (CER) induced acute renal failure (ARF) in rats. ARF was induced by intravenous injection of CER at a dose of 600 mg/kg body weight. KW-3902 at doses higher than 0.01 mg/kg (p.o.) dose-dependently attenuated the decrease of creatinine clearance and the increase of proteinuria in rats with CER-induced ARF. In contrast, furosemide and trichlormethiazide (TCM) increased urinary protein and aggravated the serum parameters. These results suggest that KW-3902 has some advantages over furosemide and TCM when used in combi nation with CER. In the diuretic study in the rats with established ARF induced by CER, KW-3902, furosemide and TCM caused a significant increase in sodium excretion, whereas acetazolamide was ineffec tive. These results suggest that the proximal tubule is functionally damaged in rats with CER-induced ARF, in accord with the histological observation demonstrating the degeneration of the proximal tubule. From the fact that KW-3902 induces diuretic action even in CER-induced ARF, it is suggested that KW-3902 acts, directly or indirectly, on the proximal tubule or other tubular sites in the kidney, resulting in the diuretic effect.

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Section: Discussionmentioning

confidence: 99%

Section: Cer-induced Arfmentioning

confidence: 99%

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Effects of KW-3902, a Novel Adenosine A1-Receptor Antagonist, on Cephaloridine-Induced Acute Renal Failure in Rats

Nagashima

Kusaka

Satô

et al. 1994

Japanese Journal of Pharmacology

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“…Studies with isolated microsomes, renal cortical slices, and isolated proximal tubules have confirmed that lipid peroxidation does occur upon Cld -':.cxp%.ure, in vitr;o, and partially explains the biochemical changes leading to Cld nephrotoxicity (6, 10, 20). Suzuki and Sudo (26,27) and Tune et a1 (32) have measured increases in the content of thiobarbituric acid-reactive substances (TBARS; presumably MDA) in renal tissue from rats and rabbits exposed to nephrotoxic doses of Cld as an index of in vivo lipid peroxidation. In the present report, there were no statistically significant changes in the tissue content of TBARS in Cld-treated animals at any time point over that observed in control animals ( Table I).…”

Section: Fig 8-continuedmentioning

confidence: 99%

Cephaloridine-Induced Renal Pathological and Biochemical Changes in Female Rabbits and Isolated Proximal Tubules in Suspension

et al. 1992

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Cephaloridine (Cld) is a nephrotoxic cephalosporin antibiotic. The intracellular biochemical changes that occur leading to Cld-induced nephrotoxicity may involve lipid peroxidation and/or mitochondria1 injury. The purpose of this report was to examine and correlate the biochemical changes induced by Cld in vivo and in vitro with the observed pathological changes in an attempt to understand better the mechanisms of@-lactaminduced nephrotoxicity. Cld treatment (500 mg/kg sc) caused elevations in blood urea nitrogen and decreases in the accumulation of p-aminohippurate (PAH) and tetraethylammonium (TEA) by renal cortical slices.Histopathological alterations, characterized by individual cell necrosis of tubular epithelial cells, were first seen 6 hr after treatment in the pars recta of the outer stripe of the medulla. Ultrastructural alterations involved the straight (S, and S,) segments of the proximal tubules. Mitochondria1 morphology was, for the most part, unaffected by Cld exposure. Cld did not cause any significant changes in tissue malondialdehyde (MDA)content in vivoat any ofthe timepointsexamined, but it didcauseadepletion ofGSH toapproximately 40% of control by 1 hr after dosing that recovered toward control by 6 hr. Significant changes were observed in renal ATP content beginning at 6 hr after treatment; however, this change mirrored the onset of histological evidence of necrosis. In isolated tubules in vitro, the onset ofglutathione (GSH) depletion and MDA formation clearly preceded lactate dehydrogenase (LDH) leakage, whereas ATP depletion was a mirror image of cell death. These data demonstrate that isolated proximal tubules in vitro are a reasonable model for Cld nephrotoxicity in rivo. Cld-induced mitochondria1 alterations leading to ATP depletion and cell injury were not observed in this study.

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Cephaloridine-Induced Inhibition of Cytochrome c Oxidase Activity in the Mitochondria of Cultured Renal Epithelial Cells (LLC-PK1) as a Possible Mechanism of Its Nephrotoxicity

Kiyomiya

Matsushita

Matsuo

et al. 2000

Toxicology and Applied Pharmacology

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Changes in lipid peroxidation and activities of xanthine oxidase, superoxide dismutase and catalase in kidneys of cephaloridine-administered rats.

Cited by 10 publications

References 30 publications

Effects of KW-3902, a Novel Adenosine A1-Receptor Antagonist, on Cephaloridine-Induced Acute Renal Failure in Rats

Effects of KW-3902, a Novel Adenosine A1-Receptor Antagonist, on Cephaloridine-Induced Acute Renal Failure in Rats

Cephaloridine-Induced Renal Pathological and Biochemical Changes in Female Rabbits and Isolated Proximal Tubules in Suspension

Cephaloridine-Induced Inhibition of Cytochrome c Oxidase Activity in the Mitochondria of Cultured Renal Epithelial Cells (LLC-PK1) as a Possible Mechanism of Its Nephrotoxicity

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