Disease relevance of Esquinon

• Carboquone (CQ) and hyperthermia (HT) are capable of preferentially killing oxygen-deficient cells, both in vitro and in vivo [1].
• Enhancement of the cytotoxicity of mitomycin C (MMC) and carboquone (CQ) by hypoxia at elevated temperature was examined using the SDI test of mouse Sarcoma 180 and Ehrlich cells and clonogenic assay of HeLa cells [2].
• We determined the correlation between DNA strand breaks and the toxicity of carboquone (CQ) in HeLa cells in vitro and in mouse sarcoma 180 (S-180) cells in vivo, using in situ nick translation [3].
• Decrease in the SD activity was noted in the colon cancer tissues, compared to the rectal cancer tissues, exposed to six antitumor drugs and in particular, to CQ (p less than 0.05), DDP (p less than 0.01) and ACR (p less than 0.05, one-sided paired t test) [4].
• At the peak plasma level, urothelial transitional-cell carcinomas were 'susceptible' to cis-platinum, carboquone, and adriamycin, the sensitivity rates being 60%, 50%, and 30%, respectively [5].

High impact information on Esquinon

• A second episode of jaundice followed the intravaginal administration of a mixture of furazolidone and nifuroxime [6].
• The effect of cysteamine and glutathione addition on the redox behaviour of metronidazole, chloramphenicol, M&B 4998, nitrofurazone, and nifuroxime has been studied by electrochemical techniques [7].
• Decrease in the SD activity was noted in the tumor tissues, compared to the tumor-adjacent normal tissues, exposed to CQ, MMC and ACR (p less than 0.01) [4].
• The resistant subline (Lu99/317) showed cross-resistance to MMC and carboquone (CQ), but not to ADR or CDDP [8].
• However, the levels of NADPH:cytochrome P450 reductase, which is another activation enzyme for MMC and CQ, were comparable in resistant and parent cell lines [8].

Chemical compound and disease context of Esquinon

• Hydralazine combined with hyperthermia enhances the effects of carboquone [1].
• The results of the chemosensitivity assay are as follows: 5-FU seems to be the most beneficial for primary colorectal cancer; carboquone (CQ), etoposide (VP-16), 5-FU, and mitomycin-C (MMC) for nodal metastasis; CQ, cisplatin (CDDP), 5-FU, adriamycin (ADR) and VP-16 for malignant effusion; and VP-16, CDDP and CQ for liver metastasis [9].
• Potentiation of the cytotoxicity of carboquone by flavone acetic acid combined with hyperthermia [10].
• The antitumor effects of liposome-encapsulated carboquone (CQ-liposome) were studied following intraperitoneal administration into mice bearing Ehrlich ascites carcinoma (EAC) [11].
• It is of special interest that 5 of the 10 patients who received the three drug infusion of Carboquone (CQ) + Mitomycin C (MMC) + Nimustine-HCL (ACNU) for squamous cell carcinoma, showed complete disappearance of viable cancer cells at the tumor site; something which was never observed after the single and two drug infusions [12].

Biological context of Esquinon

• The stability of carboquone in alcohols. II. Kinetics and mechanisms of degradation of carboquone in methanol [13].
• The effects of encapsulation of carboquone (CQ) in the liposomes were investigated on the plasma clearance and tissue distribution of CQ in rabbit and rat [14].
• Total tumor cell count and hematopoietic system of ah 109A-bearing rats treated with mitomycin C and carboquone [15].

Anatomical context of Esquinon

• Leukocyte count was decreased in the carboquone group, but no change in serum transaminase was found in either group [16].
• Carboquone was found to greatly stimulate the aerobic NADH oxidation in the presence of both the partially purified NADH-cytochrome b5 reductase and cytochrome b5 prepared from hepatic microsomes by acting as an electron carrier from cytochrome b5 to molecular oxygen [17].

Associations of Esquinon with other chemical compounds

• These tissues obtained at the time of surgery were exposed to carboquone (CQ), adriamycin (ADM), mitomycin C (MMC), aclacinomycin A (ACR), cisplatin (DDP) and 5-fluorouracil (5-FU) [4].
• By extrapolation, first half-lives in purely aqueous media were found to increase in the order: nitrofurazone, nifuroxime, chloramphenicol, metronidazole and M&B 4998 (from 8.9 x 10(-2) seconds for nitrofurazone to 98s for M&B 4998 at a radical anion concentration of 1 x 10(-6) mol/dm3) [18].
• Minimum concentrations required to elicit this unusual defect ranged from 0.01 mM with nifuroxime and furazolidone to 0.5 mM with ronidazole and were roughly correlated with single electron redox potentials; i.e., agents with relatively high redox potentials were generally more effective than those with low potentials [19].
• Tumour tissues obtained at surgery were exposed to five different anticancer drugs: carboquone (CQ), adriamycin (ADM), mitomycin C (MMC), cisplatin (DDP) and 5-fluorouracil (5-FU) [20].
• Although there were no statistical differences in drug sensitivities according to macroscopic findings (Borrmann's classification), the expanding growth type was more susceptible that the infiltrating type to cisplatin, aclacinomycin A (ACR) and carboquone (CQ) microscopically [21].

Gene context of Esquinon

• DT-diaphorase, which is one of the activation enzymes of MMC and CQ, was deficient in Lu99/317 cells as determined by enzyme activity assay [8].
• Carboquone showed enhanced cytotoxicity under hypoxia for PLC/PRF/5 alone [22].

Analytical, diagnostic and therapeutic context of Esquinon

• Combined therapeutic effects of an immunomodulator, PSK, and chemotherapy with carboquone on rat bladder carcinoma [23].
• 18 previously untreated patients with multiple myeloma were entered in a clinical study of a combination chemotherapy, carboquone (CQ) and prednisolone (P) (CQ-P) [24].
• Determination of carboquone in plasma and ascites by high performance liquid chromatography after intravenous and intraperitoneal administration in man [25].
• The oral administration of Carboquone (an analogue of mitomycin C) as maintenance therapy inhibited recurrence effectively, but produced several fatal effects such as severe anemia, infection, and intestinal bleeding [26].
• The results obtained from the studies of intraperitoneal growth of AH-109A cells pretreated with carboquone in vivo and the survival of host animals well corresponded to the extent of the damage of DNA as revealed by alkaline and neutral sucrose density gradient centrifugation [27].

References