Altered biological distribution and decreased neuromuscular toxicity of niosome encapsulated vincristine

G. Parthasarathi, N. Udupa, N. Parameshwaraiah, G. K. Pillai

Research output: Contribution to journalArticle

3 Citations (Scopus)

Abstract

Effects of encapsulation within niosomes (nonionic surfactant vesicles) on the biological distribution and toxicity of vincristine - a widely used anticancer drug have been investigated. Plasma kinetics, tissue distribution profile and neuromuscular toxicity of niosomal vincristine (NVCR) were compared with those of free vincristine (FVCR). NVCR was cleared from the plasma much more slowly [t( 1/2 )(β) = 1.388 hr] than FVCR [t( 1/2 )(β) = 0.7 4hr]. Over the 48hr period of experiment, the niosome formulation delivered significantly more drug to the plasma compartment than FVCR and resulted in reduced accumulation of drug in gut and skeletal muscle. Encapsulation caused a marked alteration in the tissue disposition of the drug. NVCR was less toxic both in terms of mortality and morbidity. Importantly, histopathological studies of skeletal muscle, spinal cord and sciatic nerve of NVCR treated albino wistar rats demonstrated the less toxic potential of encapsulated vincristine. Further, the biochemical studies, estimation of enzymes plasma creatine phosphokinase and lactate dehydrogenase, confirmed the safety profile of NVCR. The decreased partitioning of NVCR to non active sites resulted in a significant amelioration of the toxic side effects, gastrointestinal and myological in particular, of the drug. The results indicate that the delivery of vincristine by encapsulating it in niosomes offer an efficient means of decreasing its toxic effects.

Original languageEnglish
Pages (from-to)124-130
Number of pages7
JournalIndian Journal of Experimental Biology
Volume34
Issue number2
Publication statusPublished - 02-1996

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Vincristine
Liposomes
Poisons
Pharmaceutical Preparations
Skeletal Muscle
Spinal Nerves
Sciatic Nerve
Tissue Distribution
Creatine Kinase
L-Lactate Dehydrogenase
Surface-Active Agents
Wistar Rats
Catalytic Domain
Spinal Cord
Morbidity
Safety

All Science Journal Classification (ASJC) codes

  • Biotechnology
  • Medicine(all)
  • Molecular Biology
  • Cell Biology

Cite this

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title = "Altered biological distribution and decreased neuromuscular toxicity of niosome encapsulated vincristine",
abstract = "Effects of encapsulation within niosomes (nonionic surfactant vesicles) on the biological distribution and toxicity of vincristine - a widely used anticancer drug have been investigated. Plasma kinetics, tissue distribution profile and neuromuscular toxicity of niosomal vincristine (NVCR) were compared with those of free vincristine (FVCR). NVCR was cleared from the plasma much more slowly [t( 1/2 )(β) = 1.388 hr] than FVCR [t( 1/2 )(β) = 0.7 4hr]. Over the 48hr period of experiment, the niosome formulation delivered significantly more drug to the plasma compartment than FVCR and resulted in reduced accumulation of drug in gut and skeletal muscle. Encapsulation caused a marked alteration in the tissue disposition of the drug. NVCR was less toxic both in terms of mortality and morbidity. Importantly, histopathological studies of skeletal muscle, spinal cord and sciatic nerve of NVCR treated albino wistar rats demonstrated the less toxic potential of encapsulated vincristine. Further, the biochemical studies, estimation of enzymes plasma creatine phosphokinase and lactate dehydrogenase, confirmed the safety profile of NVCR. The decreased partitioning of NVCR to non active sites resulted in a significant amelioration of the toxic side effects, gastrointestinal and myological in particular, of the drug. The results indicate that the delivery of vincristine by encapsulating it in niosomes offer an efficient means of decreasing its toxic effects.",
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Altered biological distribution and decreased neuromuscular toxicity of niosome encapsulated vincristine. / Parthasarathi, G.; Udupa, N.; Parameshwaraiah, N.; Pillai, G. K.

In: Indian Journal of Experimental Biology, Vol. 34, No. 2, 02.1996, p. 124-130.

Research output: Contribution to journalArticle

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