Methylene blue prevents carbon monoxide induced-hematological and cardiac toxicity in adult female albino rats

The present study aimed to investigate the protective effect of concurrent administration of methylene blue [MB] [1mg/kg, i.p. day] on heart and blood under repeated CO intoxication [1% for 4 minutes / day] for a period up to 30 days in female adult albino rats. Animals were divided into four groups. First group is the control group where the animals admistered saline and breathed natural air. Methylene blue group, where the animals received methylene blue [MB] [1mg/kg/day, i.p]. Carbon monoxide group [CO] that inhaled carbon monoxide [CO, 1%] for 4 minutes day in a closed chamber. Carbon monoxide plus methylene group where the animals pretreated with MB followed by CO inhalation at the aforementioned doses. A group of eight rats from each group was sacrificed at time intervals of 10, 20 and 30 days. Levels of methemoglobin [met Hb] and gas analysis [P02 and PCO[2]] were measured in arterial blood. Superoxide dismutase [SOD], reduced glutathione [GSH], malondialdehyde [MDA] as oxidative stress parameters and adenosine triphosphate [AlP] content were measured in heart and blood serum. Carbon monoxide increased PCO[2] and decreased P02 levels, decreased the ATP content and increased the level of met Hb in blood in comparison to control. Moreover, CO-treated animals showed increased levels of MDA and decreased levels of GSH and SOD in blood and heart tissues. Methylene blue pretreatment significantly minimized the adverse effect of CO and restored normal levels of tested blood gases, cleans the hemoglobin [decreased met Hb], normalized the levels of ATP, GSH. The study suggests that carbon monoxide induced its harmful effects by poisoning hemoglobin and /or induction of oxidative stress. The restorative effects of methylene blue on the physiological functions might be due to the potential of MB as antioxidant and to replace CO in Rb molecule

Therapeutic drug-induced liver injury in liver biopsies

35 patients admitted to Mansoura University Hospital with the clinical picture of hepatitis were selected for the present investigation after being asked carefully for history of drug intake and examined clinically. Stool examinations were negative for Bilharzia and other parasites. Serological tests were negative for hepatitis surface antigen. Ture cut needle biopsy for liver was done for all of these patients and stained with various stains. These were one patient with history of halothain intake, 10 with history of intake of oral contraceptive, 2 with history of chlorpromazine and 20 with history of phenyl-butazone and 20 with history of isoniazid. Histologically a spectrum of lesions was recognized as a result of liver injury by these drugs. The produced lesions were categorized as follows: 1-lesion resembling viral hepatitis. 2-Cholestasis with inflammation and liver cell damage. 3-Pure cholestasis. The drugs causing each of these lesions and their differential diagnosis specially from viral hepatitis were discussed