High fat mixed lipid diet modifies protective effects of exercise on 1,2 dimethylhydrazine induced colon cancer in rats.

The aim of the present study was to evaluate the effect of long-term swimming exercise in conjunction with a high fat mixed lipid (HFML) diet on colon cancer (CC) development and lipid peroxidation in the large bowel. We used forty male Wistar rats, which were randomly divided into one control group and four cancer groups: sedentary and swimming groups fed a standard diet (LFCO) and sedentary and swimming groups fed an HFML diet. Corticosterone was determined during the experiment. After 6 months of swimming, the rats were sacrificed and blood, heart, liver, muscle and large bowel were taken for determining the activity of serum enzymes, antioxidant capacity and CC development. The results demonstrate that exercise has a protective role in CC development. Attenuated development of CC and increased levels of malondialdehyde (MDA) in the large bowel of exercised rats show that one of the protective effects of exercise on developing CC is induction of oxidative stress. However, in terms of the combined effects of dietary fat and exercise, our results indicate that the protective role of exercise on CC development is significantly depressed by an HFML diet. An HFML diet significantly reduced the protective influence of exercise on colon carcinogenesis in rats and affected the degree of peroxidation in the large bowel during exercise, as well as concentrations of serum enzymes (LDH, α-HBDH, CK, ALT and AST). Our results indicate that an HFML diet, which reflects the composition of a Western style diet, is a significant modifier of the protective effects of exercise on CC development in rats.

N-methylnitrosourea induced breast cancer in rat, the histopathology of the resulting tumours and its drawbacks as a model.

Several animal models of breast cancer have been developed to study various aspects of breast cancer biology. Substantial evidence suggests that the N-methylnitrosourea (MNU) animal model mimics human breast cancer in many respects. It has therefore been used extensively to evaluate preventive and therapeutic agents for human breast cancer. Chemically induced rodent models are also suitable for studying malignant progression. Recently, Liska et al. [7] established two protocols of MNU administration depending on the animal's age and number of applications of carcinogen, with the aim of investigating the advanced stages of mammary gland tumours. We used the same protocol as Liska but have obtained substantially different results. These results are presented and discussed in the frame of suggested key drawbacks of the MNU induced breast cancer rat model, as a contribution to the debate about the suitability of that model for evaluating preventive and therapeutic agents.

Recent advances in protection against doxorubicin-induced toxicity.

Anthracycline antibiotics are among the most effective and commonly used anticancer drugs. Unfortunately, their clinical use is restricted by dose-dependent toxicity. Doxorubicin is an anthracycline antibiotic and cytotoxic (antineoplastic) agent. It is commonly used against ovarian, breast, lung, uterine and cervical cancers, Hodgkin's disease, soft tissue and primary bone sarcomas, as well against in several other cancer types. It has been shown that free radicals are involved in doxorubicin-induced toxicity. Doxorubicin causes the generation of free radicals and the induction of oxidative stress, associated with cellular injury. This review illustrates recent applications of different natural products, drugs, drug delivery systems, and approaches for protection against doxorubicin-induced toxicity (2006-present).

Cardioprotective effects of fullerenol C(60)(Oh)(24) on a single dose doxorubicin-induced cardiotoxicity in rats with malignant neoplasm.

The therapeutic utility of the anthracycline antibiotic doxorubicin is limited due to its cardiotoxicity. Our aim was to investigate the efficacy of fullerenol C(60)(OH)(24) in preventing single, high-dose doxorubicin-induced cardiotoxicity in rats with malignant neoplasm. Experiment was performed on adult female Sprague Dawley rats with chemically induced mammary carcinomas. The animals were sacrificed two days after the application of doxorubicin and/or fullerenol, and the serum activities of CK, LDH and alpha-HBDH, as well as the levels of MDA, GSH, GSSG, GSH-Px, SOD, CAT, GR, and TAS in the heart, were determined. The results obtained from the enzymatic activity in the serum show that the administration of a single dose of 8 mg/kg in all treated groups induces statistically significant damage. There are significant changes in the enzymes of LDH and CK (p < 0.05), after an i.p. administration of doxorubicin/fullerenol and fullerenol. Comparing all groups with untreated control group, point to the conclusion that in the case of a lower alpha-HBDH/LDH ratio, results in more serious the liver parenchymal damage. The results revealed that doxorubicin induced oxidative damage and that the fullerenol antioxidative influence caused significant changes in MDA, GSH, GSSG, GSH-Px, SOD, CAT, GR, and TAS level in the heart (p < 0.05). Therefore, it is suggested that fullerenol might be a potential cardioprotector in doxorubicin-treated individuals.