Protection against cisplatin-induced lipid peroxidation and kidney damage by procaine in rats

Zhong, Laifu; Zhang, J G; M, Zhang; L, SUSEELA DEVI; Xia, Yujing

doi:10.1007/bf01971843

Cited by 29 publications

(12 citation statements)

References 8 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Previous investigations have suggest ed that CDDP-induced nephrotoxicity is related to oxida tive stress and that lipid peroxidation is one of the mecha nisms [22,23], In the present study, CDDP induced a sig nificant increase in both renal glutathione and lipid per oxide levels, 5 days after administration. This finding is compatible with the earlier work of others [24,25].…”

Section: Discussionsupporting

confidence: 52%

Effect of <i>L</i>-Histidinol on Cisplatin Nephrotoxicity in the Rat

Badary¹,

Nagi²,

Al-Sawaf³

et al. 1997

Nephron

View full text Add to dashboard Cite

The effect of L-histidinol (LHL) on the acute nephrotoxicity produced by cisplatin (CDDP; 6 mg/kg, i.v.) was investigated in the rat. Intraperitoneal administration of LHL (100 mg/kg × 5 doses, 2 h apart) starting 2 h prior to CDDP single injection produced significant protection of renal function. The attenuation of nephrotoxicity was evidenced by significant reductions in serum urea and creatinine concentrations, decreased polyuria, reduction in body weight loss, marked reduction in urinary fractional sodium excretion and glutathione-S-transferase (GST) activity, and increased urine/serum creatinine ratio as well as increased creatinine clearance. LHL significantly ameliorated the toxic renal biochemical changes induced by CDDP. Renal lipid peroxides, glutathione levels and GST activity showed a marked tendency towards the normal values. Accumulation of platinum in renal tissues was significantly decreased in the presence of LHL. It is concluded that LHL can act as a nephroprotectant, and it is suggested that it would have beneficial effects on the kidney in clinical settings.

show abstract

Section: Discussionsupporting

confidence: 52%

Effect of <i>L</i>-Histidinol on Cisplatin Nephrotoxicity in the Rat

Badary¹,

Nagi²,

Al-Sawaf³

et al. 1997

Nephron

View full text Add to dashboard Cite

show abstract

“…After digestion of the slices with 1 ml of concentrated HNO3 overnight, sodium (Na § and potassium (K +) levels were measured with a flame photometer (FLM-3, Denmark). Pt content was determined by using atomic absorption spectrophotometer (Hitachi Z-7000) as described previously (Zhong et al 1990). The remainder of the incuba- Time (minl Fig.…”

Section: Measurement Of Gluconeogenesis In Renal Cortical Slicesmentioning

confidence: 99%

“…Jackson (1984) confirmed in an in vitro study that procaine inhibited iron and ascorbate-induced lipid peroxidation of skeletal muscle homogenates. More recently, study in this laboratory showed that procaine completely inhibited CDDP-induced lipid peroxidation in vitro and in viv0 (Zhong et al 1990). The further evaluation, however, of protective effects of procaine on cytotoxicity by CDDP has not yet been reported.…”

Section: Introductionmentioning

confidence: 96%

“…However, the therapeutic dose of CDDP must be limited to avoid nephrotoxicity Offprint requests to: L. F. Zhong (Madias and Harrington 1978;Von Hoff et al 1979). Regarding the mechanisms of nephrotoxicity of CDDP, so far several hypotheses have been put forward, among which oxidative stress (including depletion of glutathione and production of lipid peroxide) is a noticeable one (Sugihara et al 1987 a, b;Hannemann and Baumann 1988;Zhong et al 1990). Hannemann and Baumann (1988) reported that CDDP inhibited gluconeogenesis in renal cortical slices in vitro.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Protection effects of procaine on oxidative stress and toxicities of renal cortical slices from rats caused by cisplatin in vitro

et al. 1992

Self Cite

View full text Add to dashboard Cite

Incubation of rat renal cortical slices with 2 mM cisplatin (CDDP) at 37 degrees C for different periods of time (15-180 min) increased malondialdehyde (MDA) formation, decreased intracellular glutathione (GSH), and inhibited gluconeogenesis in the slices. CDDP-induced MDA formation increased by 53% after 180 min of incubation and GSH decreased by 35% after 60 min of incubation. Both depletion of GSH and inhibition of gluconeogenesis preceded MDA formation. Procaine (2 mM) completely inhibited CDDP-induced lipid peroxidation without affecting depletion of GSH, but even potentiated gluconeogenesis inhibition, while 2 mM dithiothreitol (DTT) largely reversed all of these biochemical indices. After 240 min of incubation, 2 mM CDDP produced marked cytotoxicities, characterized by an increase in leakage of alkaline phosphatase (ALP) (132%), lactate dehydrogenase (LDH) (115%) and N-acetyl-beta-glucosaminidase (NAG) (157%), decrease in intracellular K+ (64%), and change in total water contents in the slices. Procaine (2 mM) showed protection against CDDP-induced cytotoxicities to a certain extent. These results suggest that depletion of GSH might be a determinant step in the oxidative stress and subsequent cytotoxicity, and that procaine is a powerful antioxidant and would be a promising drug for ameliorating some of the adverse effects of CDDP.

show abstract

“…The oxidative stress process contributes to CP-nephrotoxicity (Safirstein et al 1981;Zhong et al 1990). It has been observed that the reactive oxygen and nitrogen species can activate p38 MAPKs (Xia et al 1995;Bokemeyer et al 1996).…”

Section: Introductionmentioning

confidence: 99%