M.M. Ahmed

Gastric antiulcer and cytoprotective effect of Commiphora molmol in rats

The aqueous suspension of Commiphora molmol (oleo-gum resin) has been screened for its potential to protect gastric mucosa against the ulcers caused by 80% ethanol, 25% NaCl, 0.2 M NaOH, indomethacin and combined indomethacin-ethanol treatment. C. molmol pretreatment at doses of 250, 500 and 1000 mg/kg provided dose-dependent protection against the ulcerogenic effects of different necrotizing agents used. The effects caused by ethanol were further investigated. Treatment of rats with 1 ml of 80% ethanol was found to cause depletion of stomach wall mucus, reduction in the concentration of protein, nucleic acids and NP-SH groups in the stomach wall. Ethanol treatment also caused histopathological lesions including necrosis, erosion, congestion and haemorrhage of the stomach wall. Pretreatment with C. molmol offered a dose-dependent protection against all these effects. In the same manner it affected the malondialdehyde concentration altered by ethanol treatment. C. molmol also offered protection against mucosal damage caused by indomethacin and its combination with ethanol. The protective effect of C. molmol observed in the present study is attributed to its effect on mucus production, increase in nucleic acid and non-protein sulfhydryl concentration, which appears to be mediated through its free radical-scavenging, thyroid-stimulating and prostaglandin-inducing properties.

Evaluation of the genotoxic, cytotoxic, and antitumor properties ofCommiphora molmol using normal and Ehrlich ascites carcinoma cell-bearing Swiss albino mice

The genotoxic, cytotoxic and antitumor properties ofCommiphora molmol (oleo gum resin) were studied in normal and Ehrlich ascites carcinoma cell-bearing mice. In normal mice, the genotoxic and cytotoxic activity was evaluated on the bases of the frequency of micronuclei and the ratio of polychromatic to normochromatic cells in bone marrow, which was substantiated by the biochemical changes in hepatic cells. The antitumor activity ofC. molmol was evaluated from the total count and viability of Ehrlich ascites carcinoma cells and their nucleic acid, protein, malondialdehyde, and elemental concentrations in addition to observations on survival and the trend of changes in body weight. The tumors at the site of injection were evaluated for histopathological changes. Treatment withC. molmol (125–500 mg/kg) showed no clastogenicity but was found to be highly cytotoxic in normal mice. The results obtained in the Ehrlich ascites carcinoma cell-bearing mice revealed the cytotoxic and antitumor activity ofC. molmol which was found to be equivalent to those of the standard cytotoxic drug cyclophosphamide. On the basis of the nonmutagenic, antioxidative, and cytotoxic potential ofC. molmol as observed in the present study, its use in cancer therapy seems to be appropriate and further investigations are suggested.

Anticarcinogenic Effect of Commiphora molmol on Solid Tumors Induced by Ehrlich Carcinoma Cells in Mice

The anticarcinogenic potential of Commiphora molmol (oleoresin) was studied in Ehrlich-solid-tumor-bearing mice. The antitumor activity of C. molmol was evaluated from the total count and viability of Ehrlich solid tumor cells and their nucleic acid, protein, malondialdehyde and glutathione levels at the end of 25 and 50 days of treatment. Furthermore, observations of animal survival rate and measurements of the tumor and body weight were made. The Ehrlich solid tumors were also evaluated for histopathological changes. Treatment with C. molmol (250 and 500 mg/kg/day) was found to be cytotoxic in Ehrlich solid tumors cells. The antitumor potential of C. molmol was comparable to the standard cytotoxic drug cyclophosphamide. This effect of C. molmol was less pronounced after 50 days of treatment. The present study confirmed the cytotoxic and anticarcinogenic potential of C. molmol. Further studies are warranted to explore its mode of action and safety for medicinal use in cancer therapy.

A study of uric acid pretreatment for the protection of rat gastric mucosa against toxic damage

Uric acid was evaluated for its potential to protect the gastric mucosa against the injuries caused by 80% ethanol, 0.6 m-HCl and 0.2 M-NaOH in rats. Uric acid at doses of 50, 100 or 300 mg/kg body weight provided dose-dependent protection against the ulcerogenic effects of all three agents. Other effects caused by ethanol only were studied. Serum uric acid concentrations were statistically significantly increased by both uric acid and ethanol treatments. Treatments of rats by gavage with 1 ml 80% ethanol was found to cause depletion of stomach-wall mucus, to lower the concentrations of protein, nucleic acids and non-protein sulphydryl groups in the stomach wall, and to cause histopathological lesions, including necrosis, erosions, congestion and haemorrhage, of the stomach wall. Treatment with uric acid, at doses of 50, 100 or 300 mg/kg body weight, by gavage, provided some measure of protection against all of these effects, and the protection was generally dose dependent. The protective effects of uric acid against damage to the gastric-wall mucosa may be mediated through its effects on mucus production and non-protein sulphydryl concentrations, and/or its free-radical scavenging properties.

Effect of camel urine on the cytological and biochemical changes induced by cyclophosphamide in mice

Camel urine treatment was found to cause a significant cytotoxic effect in the bone marrow cells of mice. This cytotoxicity at higher doses was comparable with that of standard drug cyclophosphamide (CP). However, unlike CP, the camel urine treatment failed to induce any clastogenicity. The cytotoxicity induced by camel urine treatment was substantiated by the reduction of liver nucleic acids and glutathione levels and increased malondialdehyde (MDA) contents in the same animals. CP treatment was found to be highly clastogenic, cytotoxic and it reduced the levels of nucleic acids, proteins, glutathione and increased malondialdehyde concentration due to its prooxidant nature. The non-clastogenic nature of camel urine was attributed to the antioxidant and antimutagenic compounds present in camel urine. Pretreatment with camel urine increased the cytotoxicity of CP and intensified the CP induced reduction of liver nucleic acids, glutathione and increased the MDA concentration. The increase of CP induced cytotoxicity appears to be partly due to the additive effect of the two treatments on cellular lipid peroxidation.

Effect of Caralluma tuberculata on the cytological and biochemical changes induced by cyclophosphamide in mice.

Treatment with Caralluma tuberculata extract induced complex biochemical and cytological changes in mice. Its cytotoxicity in the bone marrow cells of mice was comparable with that of the standard drug cyclophosphamide (CP); however, unlike CP, C. tuberculata was not clastogenic (as shown by the micronucleus assay). A dose-dependent decrease in the RNA content of liver and testes was produced by C. tuberculata treatment whereas there was no effect on the content of nucleic acid and protein in the brain. In the extract-treated animals there was a significant and dose-dependent increase in the DNA content of the liver, with a negligible effect on the protein content. Combined treatment with C. tuberculata and CP showed that C. tuberculata diminished the effect of CP on DNA levels; however, RNA levels were further suppressed, resulting in increased cytotoxicity. Pretreatment with C. tuberculata extract significantly reduced the clastogenicity of CP. These results indicated the involvement of different phytoconstituents acting by different routes.

Effect of Alpinia galanga Treatment on Cytological and Biochemical Changes Induced by Cyclophosphamide in Mice

AbstractAn ethanol extract of Alpinia galanga was administered to mice. This treatment did not affect the number of micronucleated polychromatic erythrocytes (PCE) in bone marrow cells, alter the protein and nucleic acid contents in liver and testes, or cause mitodepression of bone marrow. Cyclophosphamide (CP) induced micronucleated PCE, and A. galanga treatment significantly reduced this effect without altering cytotoxicity. The minimum effective dose of A. galanga extract required to produce this effect was 125 mg/kg body weight. Biochemical changes caused by CP-treatment in the liver of treated animals were also significantly inhibited by A. galanga treatment.