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At least 271 records · Page 15Linked to original sources
PubMed1993

Cytotoxic effect of thiacarbocyanine dyes on human colon carcinoma cells and inhibition of bovine heart mitochondrial NADH-ubiquinone reductase activity via a rotenone-type mechanism by two of the dyes.

Five lipophilic-cationic thiacarbocyanine compounds differing in the side chains (methyl-S13, ethyl-S23, propyl-S33, butyl-S43, and pentyl-S53) and a related thiadicarbocyanine compound with ethyl side chains (S25) exhibited a selective cytotoxic effect on human colon carcinoma cells compared to green monkey kidney epithelial cells. The inhibitory concentration for 50% inhibition of growth (IC50) for the carcinoma cells ranged from 13 nM for S13 and S23 to 160 nM for S25. The carcinoma cells were 4- to 100-fold more sensitive than the normal cells. Two of the five compounds, S13 and S23, selectively inhibited NADH oxidase activity with bovine heart submitochondrial particles (SMP). There was no discernable inhibitory effect by the other three thiacarbocyanine compounds on electron transport chain activity. The primary site of inhibition within the respiratory chain for S13 and S23 appeared to be the NADH to coenzyme Q portion of the mitochondrial electron transport chain. Artificial electron acceptors for this segment of respiratory chain were used to localize the inhibitory site. Using SMP, both S13 and S23 inhibited reduction of menadione, duroquinone, and coenzyme Q. Using purified complex I (NADH-ubiquinone reductase) (EC 1.6.99.3), S13 slightly inhibited reduction of juglone, duroquinone, and coenzyme Q, whereas S23 had no effect on any of the substrates. When rotenone-saturated SMP were used, the inhibitory effects of S13, but not S23, on the reduction of menadione were abolished, as was the inhibitory effect of S13 on coenzyme Q reduction when rotenone-insensitive complex I was used as the source of the enzyme. These results suggest that (1) S13 and S23 inhibition of NADH-ubiquinone reductase activity is enhanced by the membrane environment of the enzyme, and (2) the inhibition appears to be in part akin to the inhibiting mode of rotenone.

Animals↗
PubMed1990

Chemosensitivity testing of fresh human leukemia cells using both a dye exclusion assay and a tetrazolium dye (MTT) assay.

Chemosensitivity testing using a DEA was performed on 91 leukemia samples from 70 patients with leukemia. In 55 patients, comparison of in-vitro results with actual response of the patient was made. There was good correlation in 82% of the cases, the results being highly significant p less than 0.001. The MTT assay was also adapted for the chemosensitivity testing and the usefulness of this assay was evaluated by comparing the results to the DEA for 24 of the samples. Survival results produced by the two assays were very similar. The MTT procedure was also found to be equally effective as the DEA as a predictive assay of chemosensitivity.

Antineoplastic Agents↗
PubMed1988

A new way to carcinogenicity of azo dyes: the benzenediazonium ion formed from a non-aminoazo dye, 1-phenylazo-2-hydroxynaphthalene(Sudan I) by microsomal enzymes binds to deoxyguanosine residues of DNA.

1-Phenylazo-2-hydroxynaphthalene (Sudan I) activated by pre-incubation with microsomal enzymes of rat livers covalently binds to DNA from calf thymus. Benzenediazonium ion formed from Sudan I by activation with microsomal enzymes is the principal active metabolite, which binds to DNA. Enzymatic hydrolysis of modified (14C-labelled) DNA, followed by separation of deoxynucleosides on a Sephadex G-10 column revealed that deoxyguanosine is the principal target for the binding of activated Sudan I. The high-performance liquid chromatographic (HPLC) analysis indicate that probably more than one radioactive adduct of activated Sudan I with deoxyguanosine is formed.

Animals↗
PubMed1993

Photochemical treatment with the lysosomally localized dye tetra(4-sulfonatophenyl)porphine results in lysosomal release of the dye but not of beta-N-acetyl-D-glucosaminidase activity.

Tetra(4-sulfonatophenyl)porphine (TPPS4) sensitizes cells to photoinactivation mainly through formation of singlet oxygen. In human cervix carcinoma cells of the line NHIK 3025 TPPS4 localizes to a large extent in lysosomes as previously shown by fluorescence microscopical and spectroscopical techniques. In the present study photodamage to lysosomes was investigated. This was accomplished by measuring the activity of the lysosomal marker enzyme beta-N-acetyl-D-glucosaminidase (beta-AGA) after photochemical treatment (PCT). beta-AGA activity was highly sensitive to light exposure in the presence of TPPS4. The enzymatic activity was reduced by approximately 70% by non-lethal doses of photochemical treatment, indicating that inactivation of lysosomal hydrolases is not likely to contribute significantly to the cytotoxic effects of PCT. Centrifugation studies showed that TPPS4, but not beta-AGA activity, was released from lysosomes after light exposure. 20-30% of the total beta-AGA activity was resistant to the photochemical treatment. This was due to beta-AGA activity in Golgi-derived vesicles (4-5%) and in vesicles with similar density as lysosomes but not containing TPPS4. The present results indicate that lysosomal hydrolases are inactivated by photochemical treatment before they eventually escape the lysosomal compartment.

Acetylglucosaminidase↗