Attenuation of withdrawal signs, blood cortisol, and glucose level with various dosage regimens of morphine after precipitated withdrawal syndrome in mice

Morphine withdrawal usually results in unsuccessful outcomes. Despite partial benefits from alternative substances such as methadone, its use may not lead to the desired result due to the lack of mental tranquility during the withdrawal period. In this study, by means of an animal model, morphine itself was used to manage morphine dependence. Forty mice were divided into 5 groups, in which 4 groups became dependent by increasing daily doses of morphine for 7 days [15-45 mg/kg]. Afterwards, the animals received morphine for 14 days by either of the following regimens: - Once daily 45 mg/kg [positive controls]. - Increasing the interval [each time 6 hours longer than the previous interval]. - Irregular interval in every 36, 12 and 24 hours until the 21[th] day. - 12, 24, 36 hours decreasing doses [each time 2.5 mg/kg less than the former dosage]. Negative controls received saline solution only. On day 22, total withdrawal index [TWI] was determined by injecting 3 mg/kg of naloxone. Thereafter, blood samples were taken for the measurement of cortisol and glucose levels. TWI significantly decreased in all test groups in comparison with the positive control animals [P<0.001]. Cortisol levels significantly decreased when either the dosage or the administration frequencies were decreased on a regular and gradual basis [P<0.005]. Blood glucose levels significantly decreased in animals that received decreasing doses of morphine [P<0.005]. This study suggests that no other measures may be required in clinical practice except for changing the dosage regimen of morphine for the cessation of self-administration

Protective effects of captopril against aflatoxin B1-induced hepatotoxicity in isolated perfused rat liver

The liver is the major target organ for aflatoxin B1 [AFB1]. Ingestion of aflatoxin causes hepatotoxicty. In this study, captopril as new agent to help the hepatotoxicity induced by aflatoxin was suggested. The isolated perfused rat liver [IPRL] was chosen for evaluating hepatic function. Sixteen rats were divided randomly into four experimental groups: control, captopril, AFB1 and AFB1 + captopril. The level of glutathione content and lipid peroxidation, as marker of oxidative stress and lactate dehydrogenase [LDH], alanine transaminase [ALT] and aspartate transaminase [AST] activities and pH of the perfusate medium were measured. There was a significant decrease in lipid peroxidation and same increase was observed in glutathione level. Treatment with captopril also modulated the enzymes activity and pH of perfusate. This study showed that captopril protects the hepatotoxicty induced by AFB1. Therefore, this drug may provide an effective new strategy to reduce of aflatoxins toxicity