Methotrexate (MTX) is an anti-folate used to treat cancer and some inflammatory diseases. The efficacy of MTX is often limited by its severe toxicity. Propolis is one of the most significant bee products that has an important role in balancing antioxidant systems and has an anti-peroxidant effect on several tissues. The present study was conducted to investigate the ameliorative effect of propolis against the methotrexate induced oxidative damage on blood, liver and kidney in rats. A total of one hundred and twenty male Wistar albino rats of mean body weights 90 ± 5 g were divided into 5 groups. Rats were administered their respective doses of propolis and/or MTX for 3, 6 and 9 weeks intervals. Control groups (G 1 and G 2), propolis group (G 3), methotrexate group (G 4) and methotrexate and propolis co-administered group (G 5).The results showed that the MTX significant reduced hemoglobin concentration, hematocrit %, MCHC value, RBCs, WBCs and platelets count and significantly increased MCV and lymphocytes %. Moreover, it caused a significant increase in MDA level and significant decrease in GSH concentration in liver tissue as compared to normal control group (G 1) in a time dependent manner. MTX administration also caused significant increase in serum AST, ALT and ALP activities in a time dependent manner, but a significant increase in total bilirubin only in 9 weeks as compared to normal control (G 1). On the other hand, MTX impaired kidney function as reflected by a significant increase in serum urea and creatinine levels and decrease in serum uric acid level as compared to normal control group. Results suggest that administration of propolis extract (G 5) help reduce the deleterious effects due to MTX injection in a time dependent manner, whereas, administration for 9 weeks offers better alleviation over 6 or 3 weeks. Data showed that long term administration of MTX for 9 weeks produce maximum damage over 6 or 3 weeks. Propolis extract administration also recovered the structural and functional integrity of the hepatic cells.

This study was conducted to investigate the effect of manganese toxicity by manganese chloride (MnCl 2) on the experimental animals and to evaluate the efficacy of phytic acid and/or ascorbic acid in attenuating the deleterious effect induced by manganese toxicity. For this purpose, thirty healthy rabbits weighing 1655±367.07g were divided into five groups each of six rabbits. Group 1; rabbits fed on commercial diet and normal water served as normal control; group 2; rabbits fed on commercial diet and received 200 mg/L of MnCl 2 in drinking water. Group 3; rabbits received MnCl 2 in drinking water (200mg/L) and fed on commercial diet supplemented with phytic acid (20 g /kg diet). Group 4; rabbits fed on commercial diet and received 200 mg/L MnCl 2 in drinking water and orally administrated with ascorbic acid (30mg/kg body weight daily). Group 5; rabbits received MnCl 2 in drinking water (200mg/L) and fed phytic acid (20 g /kg diet) and orally administrated ascorbic acid (30mg/kg body weight daily) by intragastric tube. Results showed that MnCl 2 intoxication significantly reduced haemoglobin (Hb) concentration and serum iron with a significant increase in total iron binding capacity. Also, it induced a significant increase in malondialdehyde (MDA) level accompanied by a significant decrease in reduced glutathione (GSH) concentration and superoxide dismutase (SOD) activity. Moreover, MnCl 2 intoxication caused a significant increase in serum alanine transaminase (ALT), aspartate transaminase (AST) activities. Also, serum urea and creatinine significantly elevated in MnCl 2-intoxicated group. An improvement was noticed in these altered parameters after oral administration of phytic acid and/or ascorbic acid.

Introduction: Ovariectomies rats were used to assess the preventive effects of almond and primrose oils on their lipid and neurochemical profiles. Methods: The experimental groups were as follows: Group 1: A negative control group. Group 2: Rats given an oral dose of almond oil (800 mg/kg/d) for 30 days. Group 3: Rats given an oral dose of primrose oil (500 mg/kg/d) for 30 days. Group 4: Untreated ovariectomized rats. Group 5: Ovariectomized rats given an oral dose of almond oil (800 mg/kg/d) for 30 days. Group 6: Ovariectomized rats given an oral dose (500 mg/kg/d) of primrose oil daily for 30 days. Results: Oral administration of almond and primrose oils significantly decreased mean (P < 0.05) serum total cholesterol (TC), triacylglycerol (TG), low-density lipoprotein cholesterol (LDL-C), and very low-density lipoprotein cholesterol (VLDL-C) concentrations and raised high-density lipoprotein cholesterol (HDL-C) in the ovariectomized groups compared to group 4 (P < 0.05). They also increased leptin and estradiol (E2) concentrations in groups 5 and 6. Administration of oils showed a marked increase in noradrenalin, dopamine, and 5-hydroxytyramin levels and a marked decrease in PGE2 and COX-2 levels (P < 0.05). Rats given almond and primrose oils revealed minor capillary congestion in the hippocampus in brain sections. Conclusion: Administration of almond or primrose oils may improve central nervous system functions and decrease the risk of cardiovascular illnesses. They also might be effective against atherosclerosis, inflammation, endocrine disorders, and cognitive impairments for women who undergo surgical menopause prior to their natural menopause.