Protective effects of cyclodextrin sulphates against gentamicin-induced nephrotoxicity in the rat

Uekama, Kaneto; Shiotani, Kazufumi; Irie, Tetsumi; Ishimaru, Yasuji; Pitha, Josef

doi:10.1111/j.2042-7158.1993.tb07100.x

Cited by 21 publications

(9 citation statements)

References 9 publications

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“…Branched CyDs, 23,24,[164][165][166] b-CyD sulphate [167][168][169] and sulfoalkyl ethers of CyDs 122) may be a new class of parenteral drug carriers because they are highly hydrophilic and less hemolytic than parent and other hydrophilic CyDs. When insulin solutions containing SBE4-b-CyD were injected into the dosal subcutaneous tissues of rats, the plasma immunoreactive insulin (IRI) level rapidly increased and maintained higher IRI levels for at least 8 h (Fig.…”

Section: Absorption Enhancement By Hydrophilic Cydsmentioning

confidence: 99%

Design and Evaluation of Cyclodextrin-Based Drug Formulation

2004

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Section: Absorption Enhancement By Hydrophilic Cydsmentioning

confidence: 99%

Design and Evaluation of Cyclodextrin-Based Drug Formulation

2004

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“…[35][36][37][38][39][40][41][42][43][44] In addition, they have heparin-like activity resulting in an increase in blood clotting times which limits the cyclodextrin dose that can be administered to patients. Therefore, the use of sulfated cyclodextrins as potential complexing agents will not be discussed further.…”

Section: Table 1sgeneral Structures a Of Cyclodextrins Referred To Inmentioning

confidence: 99%

Pharmaceutical Applications of Cyclodextrins. 2. In Vivo Drug Delivery

Rajewski¹,

Stella²

1996

Journal of Pharmaceutical Sciences

759

374

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The objective of this Review is to summarize and critique recent findings and applications of both unmodified and modified cyclodextrins for in vivo drug delivery. This review focuses on the use of cyclodextrins for parenteral, oral, ophthalmic, and nasal drug delivery. Other routes including dermal, rectal, and pulmonary delivery are also briefly addressed. This Review primarily focuses on newer findings concerning cyclodextrin derivatives which are likely to receive regulatory acceptance due to improved aqueous solubility and safety profiles as compared to the unmodified cyclodextrins. Many of the applications reviewed involve the use of hydroxypropyl-beta-cyclodextrins (HP-beta-CDs) and sulfobutylether-beta-cyclodextrins (SBE-beta-CDs) which show promise of greater safety while maintaining the ability to form inclusion complexes. The advantages and limitations of HP-beta-CD, SBE-beta-CD, and other cyclodextrins are addressed.

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“…Piperacillin has a protective role in gentamicin nephrotoxicity [14], possibly from a mechanism that involves interference with renal tubular uptake of gentamicin. Cyclodextrin sulfate also showed protection from gentamicin nephrotoxicity [42]. …”

Section: Discussionmentioning

confidence: 99%

Melatonin, a Pineal Hormone with Antioxidant Property, Protects against Gentamicin-Induced Nephrotoxicity in Rats

Shifow

Kumar²,

Naidu³

et al. 2000

Nephron

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The present study investigated the effects of melatonin, an antioxidant, on gentamicin-induced nephrotoxicity in rats. Melatonin (5 mg/kg p.o.) was used 3 days before and 8 days simultaneously with gentamicin (80 mg/kg i.p.) Saline-treated animals served as controls. Determinations of urinary creatinine, N-acetyl-β-D-glucosaminidase, glucose, protein, blood urea, serum creatinine, plasma and kidney tissue malondialdehyde (MDA), and antioxidant enzyme levels in kidney tissue were done after 8 days of gentamicin treatment. The kidneys were also examined for morphological changes using histological techniques. Gentamicin caused nephrotoxicity as evidenced by marked elevation in blood urea and serum creatinine. Mean blood urea and serum creatinine levels were 289 ± 50, and 2.5 ± 0.5 mg/dl, respectively, in rats treated with gentamicin. Melatonin significantly protected the rats from gentamicin-induced nephrotoxicity; blood urea and serum creatinine levels were 23 ± 2.7 and 0.88 ± 0.19 mg/dl, respectively. The creatinine clearance was decreased with gentamicin treatment (0.048 ± 0.007 ml/min) as compared with controls (0.41 ± 0.08 ml/h/kg). In rats treated with melatonin plus gentamicin, the creatinine clearance was similar to controls (0.41 ± 0.08 ml/h/kg). The product of lipid peroxidation (MDA) was markedly increased in plasma (2.10 ± 0.15 nmol) and kidney tissue (8.87 ± 3.2 nmol/mg protein) with gentamicin treatment. Melatonin prevented the gentamicin-induced rise in plasma MDA (1.03 ± 0.27 nmol) and kidney tissue MDA (2.57 ± 0.87 nmol/mg protein). An increased excretion of urinary N-acetyl-β-D-glucosaminidase, glucose, and protein by gentamicin was also prevented by melatonin. Kidneys from gentamicin-treated rats showed tubular epithelial loss with intense granular degeneration involving more than 50% of renal cortex, while there were findings comparable to controls in melatonin plus gentamicin treated rats. The present study indicates that melatonin significantly protects against gentamicin-induced renal toxicity in Wistar rats.

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Protective effects of cyclodextrin sulphates against gentamicin-induced nephrotoxicity in the rat

Cited by 21 publications

References 9 publications

Design and Evaluation of Cyclodextrin-Based Drug Formulation

Design and Evaluation of Cyclodextrin-Based Drug Formulation

Pharmaceutical Applications of Cyclodextrins. 2. In Vivo Drug Delivery

Melatonin, a Pineal Hormone with Antioxidant Property, Protects against Gentamicin-Induced Nephrotoxicity in Rats

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