Studies on the cytotoxic, biochemical and anti-carcinogenic potentials of ninhydrin on Ehrlich ascites carcinoma cell-bearing Swiss albino mice

Citation
S. Qureshi et al., Studies on the cytotoxic, biochemical and anti-carcinogenic potentials of ninhydrin on Ehrlich ascites carcinoma cell-bearing Swiss albino mice, INV NEW DR, 18(3), 2000, pp. 221-230
Citations number
27
Categorie Soggetti
Pharmacology,"Pharmacology & Toxicology
Journal title
INVESTIGATIONAL NEW DRUGS
ISSN journal
01676997 → ACNP
Volume
18
Issue
3
Year of publication
2000
Pages
221 - 230
Database
ISI
SICI code
0167-6997(200008)18:3<221:SOTCBA>2.0.ZU;2-F
Abstract
Ninhydrin (2,2-dihydroxy-1,3-indane dione) was evaluated for its antitumor and cytotoxic properties in Ehrlich ascites carcinoma cell (EAC Cell)-beari ng mice. The rationale behind this study has been mainly the literature rep orts of its characteristic interference with DNA synthesis and calcium home ostasis. Antitumor activity was evaluated from the total count and viabilit y of EAC cells in addition to their nucleic acid, protein, non-protein sulf hydryls (NP-SH) and malondialdehyde (MDA) contents. The EAC cell-bearing an imals were also observed for the effect on their survival and body weight v ariations. In addition, the tumors grown at the site of injection were eval uated for histopathological changes. Ninhydrin treatments (5, 10 and 20 mg/ kg/day) abate the increase in body weight and advanced the duration of surv ival in EAC cell-bearing mice. The results on histopathological investigati ons show retardation in tumor growth, decreased frequency of mitotic figure s and hair follicles and an increased necrosis in the tumor by ninhydrin tr eatment. Our results on cytotoxicity, which demonstrated compression in the number of EAC cells and their viability substantiate these data. The resul ts of biochemical studies on EAC cells exhibit a reduction in the levels of DNA, RNA, proteins and NP-SH with a subsequent increase in the concentrati ons of MDA after ninhydrin treatment. Inhibition in tumor growth was dose d ependently significant with the same dose regimen. The observed cytotoxic a nd antitumor activity of ninhydrin was comparable to cyclophosphamide. The possible mode of action of ninhydrin-induced cytotoxic and antitumor activi ty appear to be due to its interference with mitochondrial function resulti ng in inhibition of DNA synthesis, an effect that is being investigated fur ther.