Effect of paracetamol on gastric erosions induced by indomethacin in rats

Gastric mucosal injury induced by application of indomethacin, as a nonsteroidal anti inflammatory drug [NSAID], is a well- documented phenomenon. This study examined the effect of acetaminophen [paracetamol] on indomethacin. - induced gastric erosions. One hundred adult albino rats of both sexes. weighing 200-250 gm were divided into two main groups. including a group of 10 rats acts as a control. The first group was to study the effect of a single oral dose of indomethacin. paracetamol and both drugs on the gastric mucosa. and the second group was to study the effect of repeated administration of each drug and both drugs together. The animals were killed and the histopathological changes of the stomach were examined microscopically. Single therapeutic dose of indomethacin was found to induce multiple gastric erosions which these were more markced after repeated administration of the drug. Single dose or prolonged administration of paracetamol were followed by very minimal changes in the gastric mucosa. Simultaneous administration of both drugs was found to reduce the pathological lesions induced by indomethacin alone, whereas the pretreatment with paraceramol one hour before a single oral dose of ndomethacin did not affect its erosive activity. Post - treatment with paracetamol reduces the erosive effect of indomethacin either in a single dose or after repeated administration. The pathogenesis of gastric erosions and ulcers was believed to he due to prostaglandin inhibition. Indomethacin was known as a potent inhibitor of prostaglandin synthesis, whereas paracetamol is a very weak inhibitor of prostaglandin production. It is also found that paracetamol had a protective action against the erosive effect of indomethacin and this appears to be mediated by mucosat regeneration, probably resulting from increased production of mucosa growth factors. So, the use of paractamal as antipyretic and analgesic drug is recommended instead of indomethacin. or they are administrated simultaneously with or after indomethacin when there is a possibility of gastric mucosal injury, especially in prolonged treatment

Spermatogenic toxicity of vinblastine in albino rats

Since chemotherapeutic drugs are widely and progressively used in the treatment of many malignancies, the present study was planned to investigate spermatogenic toxicity [as an unavoidable side effect] of the chemotherapeutic "vinblastine" in rats in order to minimise spermatogenic toxicity as much as possible. Fifty adult male rats [each weighing 150-200 g] were classified into five groups. The first group was used as a control group being injected intraperitoneally [I.P.] with a special solvent for vinblastine [0.15 ml/100 gm body weight "B.W."] once weekly for two weeks. The remaining four groups were given vinblastine dissolved in its solvent in doses of 0.5, 1, 1.5 and 2 mg/kg B.W. by the same route for the same period. One week after the last dose, animals were sacrificed, their testes were weighed and then processed for examination by light microscopy. Testes of treated rats showed progressive decline in their weights with increasing the dose. Histopathological microscopy revealed ascending grades of disturbed spermatogenesis i.e. dose dependent toxicity. It could be concluded from the present study that minimising the dose of the chemotherapeutic vinblastine to 0.5 mg/kg B.W. reduces its spermatogenic toxicity to minimum