Evaluation of the potential protective effect of captopril against doxorubicininduced cardiotoxicity in rats

The purpose of this study was to investigate the possible protective effect of Cap, an angiotensin-converting enzyme inhibitor with an antioxidant property, against DOXinduced cardiotoxicity. Results of the present study showed that DOX decreased significantly plasma activities of CK, CK-MB and LDH, while it produced a significant increase in serum NO level, cardiac MDA level and CAT activity. Significant reductions in cardiac GSH level and GPx activity were also produced. Administration of Cap one hour before DOX treatment attenuated the reduction in CK-MB activity. The combined treated group showed significant decrease in cardiac MDA level. Also, DOX concentration was markedly decreased in both serum and cardiac tissue. Data of the present study showed that Cap had limited protective effect on cardiotoxicity produced by DOX treatment. The mechanism by which Cap exerts its protective effect may involve inhibition of lipid peroxidation

Protective effect of magnesium sulfate against radiation-induced heart damaged in albino rat

ability of Magnesium sulfate to reduce the severity of the late stage of radiation - induced heart disease [RIHD] was assessed in 40 white albino rats. Ten rats served as a control not exposed to radiation [cont.], another 10 rats were given only MgSo4 for 10 days as a negative control [-ve cont.]. The remaining rats were divided into two groups, group [A] ten animals exposed to a single dose of radiation [20 Gy]. Group [B] ten rats received MgSO4 [50 mg / kg intraperitoneally injected], 4 days prior to radiation, at the day of radiation and on the following 5 consecutive days. At 100 days post - radiation, the severity of the late state was determined by microscopic examination for myocardial fibrosis and by studying the ultrastructural changes. Irradiation found to have aggravated structured effect on the heart in the form of lysis and indistinct striation of muscle fibers, irregular pyknotic nuclei, depletion of glycogen granules and abnormal shaped mitochondiria. The adjacent cardiac muscle fibers were widely separated with marked congestion of the blood capillaries and interstitial cellular infiltration. Magnesium sulfate appeared to have protective effect in the form of reduction of myocardial of collagen content [fibrosis]. Suppression of the inflammation with preservation of the normal characters of most of the muscle fibers

protective effect of electric shock therapy on myotoxicity and cardiotoxicity of Egyptian Naja nigricollis snake venom in albino rat

The Egyptian Naja nigricollis snake is one of the most dangerous snakes. Its danger is attributed to its highly toxic venom which has severe local and systemic reactions. In the present study the use of electric shock [high voltage low amperage] therapy for the treatment of venomous snake bite was investigated. 80 adult male albino rats were divided equally into 4 groups. By intramuscular [IM] injection into the right thigh group 1 and 2 received injection of saline [solvent]. Group 3 and 4 received IM injection of LD50 of the venom [1.15mg/Kg]. After 5 minutes group 21 and 4 received electric shock therapy delivered from stun gun [5 shocks, 2 seconds each with 10 seconds interval] at the site of IM injection. In the different studied groups ECG changes were monitored throughout the study which extends for 2 hours then the rats were sacrificed. The injected muscle and heart were prepared for light and electron microscopic examinations. The histopathological, ultrastructural and ECG changes in this study revealed that the administration of a singe dose [LD50] of the venom [Gr3] induced severe myotoxicity [degeneration, necrosis and swollen mitochondria of the injected muscle], cardiotoxicity [congestion, necrosis and swollen mitochondria of the myofibrfils] with arrythmias, ischemic manifestations and lethality compared to the control [Gr1] and shock [Gr2] trated groups which showed normal patterns. This severe myotoxicity, caradiotoxicity and lethality were markedly reduced in the shock/venom treated group [Gr4]. In conclusion the high voltage shock therapy by Stun gun has a protective effect against the venom induced myotoxicity cardiotoxicity and lethality

Preliminary toxicological evaluation of salicyl hydroxamic acid in rats and dogs

Salicyl hydroxamic acid [SHAM] has been found to prevent and treat urinary stones caused by urea splitting hacteria. The present work aims at delineation of its acute toxicity in rats and dogs and its organotropic toxic potential in rats. The obtained results showed that in rats, the oral LD50 of SHAM was 5.0 [3.74 - 7.20] g/kg, while the i.p. LD50 was 0.60 [0.44 - 0.82] g/kg. Administration of 1800 mg.i.p. in dogs resulted in reversible allergic-like skin reactions. The 90 days oral toxicity study of 200 and 500 mg/kg in rats resulted in increased body weight and fluctuations in blood glucose, in addition to hepatic, renal, splenic, and cardiac toxicological and biochemical reactions. Subacute exposure to SHAM in rats has resulted in significant changes in brain amino acid neurotransmitters and an immunosuppressant effect on serum IgG. The obtained results rate are to be utilized for planning of the full preclinical toxicological evaluations

Severe adriamycin cardiotoxicity at cumulative dose below 500 Mg/M2: case report and review of the literature

Adriamycin [doxorubicin hydrochloride], an anthracycline antibiotic originally isolated from the fungus Streptomyces peucetius, is an effective antineoplastic agent against many human neoplasms including leukemias, lymphomas, and many solid tumors such as soft-tissue sarcomas. The most serious and total dose-limiting toxicity of Adriamycin is a well-described cardiomyopathy which is thought to be secondary to myocardial damage produced by oxygen-free radical production generated by the drug. The incidence of Adriamycin-induced cardiac toxicity [AICT] is directly related to the cumulative dose of the drug and is rare at cumulative doses below 550 mg/m[2] of body surface area. In this report we describe a patient who developed severe Adriamycin-induced cardiomyopathy at a cumulative dose of less than 500 mg/m[2]. The possible role of other chemotherapeutic agents which the patient was also receiving is also discussed