Background & Objective: Acetaminophen is a widely used analgesic and antipyretic drug which can produce hepatic injury in both humans and animals when given in high doses. Liver damage induced by actaminophen depends on cytochrome P-450 activities which appears as centrilobular necrosis. In this study, hepatoprotective effect of Curcuma longa (CL) is tested. The active constituent of CL is known as curcumin which has detoxifying and antioxidant activity.
Materials & Methods: 58 NMRI male mice were randomly divided into 7 groups. After an overnight denial of food, the first three groups received the following: group C normal saline, groug B 1000 mg/kg CL extract, group A 700 mg/kg oral acetaminophen. Treatment groups received acetaminophen and CL extract concurrently in various doses of 200 mg/kg, 400 mg/kg, 800 mg/kg, 1000 mg/kg, respectively. After 24 hours blood samples were taken from jugular arteries for bioassay tests and the liver was removed and placed in 10% formalin for histopathologic assessments.
Results: Serum levels of hepatic transaminases (ALT, AST) in groups receiving CL declined remarkably compared to positive control group with a significant difference (p<0.05). Based on histopathologic survey hepatic necrosis decreased as the CL intake increased.
Conclusion: Based on the present research results, CL extract improves the condition in acetaminophen-induced hepatic toxicity and its administration is recommended.

Background and Objectives: Apoptosis (programmed cell death) is an important regulatory event in spermatogenesis. Abnormally accelerated apoptosis in germ cells, may lead to an imbalance between cell proliferation and death, resulting in impairment in spermatogenic. Some studies have  shown that glucocorticoids affect testialar homeostasis by decreasing of testosterone level. In the present study, the influence of dexametasone (Dex), a widely used glucocorticoid agent, on expression of FasL (Fas-Ligand) protein (a proapoptotic protein) in mouse testicular germ cells is investigated.
Materials and Methods: Twenty-four adult male (6- 8 weeks) mice were randomly divided into 3 groups. The first and second test groups received 2 and 7 mg/kg Dex per day, respectively, for 7 days. The control group received only saline daily for 7 days. One day after the final injection, the mice were sacrificed and the test groups were placed in formalin solution for immunohistochemistry studies. Positive immunoreactivity was calculated by H-score method.
Results: The results revealed that expression of FasL in seminiferous epithelium is spermatogenic stage dependent, and the stage VII was the most susceptible to Dex. FasL expression was observed only at stages VII-VIII of spermatogenic cycle in 2 mg/kg Dex treated group (P<0.05). H-score was significantly increased in all stages of 7 mg/kg Dex treated group (P<0.05). The number of spermatocytes decreased significanhy in this group.
Conclusions: It appears that glucocorticoid agents such as Dex, induces apoptosis by affecting proapoptotic proteins.

Background and Objective: Metformin is a widely used medicine for treatment of type 2 diabetes. In this study, the effect of various doses of metformin on the mouse islets of langerhans volume was investigated.
Materials and methods: Twenty four C57BL/6 adult male mice weighting 30±5 gr were randomly divided into 4 groups. Normal saline was given to the control group (group 4) and the experimental groups (groups 1-3) received 75, 150 and 300 mg/kg metformin daily by intraperitoneal injection for seven days. One day after the last injection the mice were sacrificed by cervical dislocation and their pancreases were fixed in 10% formalin for histological studies. The volume of the islets of langerhans was estimated by using Cavalieri method.  
Results: Volume of the islets of langerhans in doses of 75 and 150 mg/kg Metformin showed a non-significant difference in comparison to control group (P>0.05). 300 mg/kg metformin treated mice showed a significant increase in islets of langerhans volume compared to the control group (P<0.05).
Conclusion: Metformin increases in the islets of langerhans volume in a dose-dependent manner. Increasing effects of Metformin on the islets of langerhans volume may be due to proliferation or hypertrophy of beta cells.