Background: Cigarette smoking is one of the 10 greatest contributors to global death and disease. Cigarette smoking is the most common type of tobacco use. In average, to date 47.5% of men and 10.3% of women are current smokers. Tobacco continues to be the second major cause of death in the world. It consists of many chemicals, including cytotoxic, carcinogenic and free radicals, therefore it affects many organs if not all. Objective: The aim of this study is to assess the extent of adverse effect of cigarette smoking on blood pressure, liver function, and hemoglobin concentration in male population on the West Coast of Libya. Methods: This study was conducted on (200) healthy male subjects, their ages ranged from 15 to 85 years. They were divided into four groups; 50 non-smokers as control group (age between 15-35 years), 50 smokers (age between 15-35 years), 50 non-smokers as control group (age between 36-84 years) and 50 smokers (age between 36-84 years). The blood was collected in EDTA tubes to test the Complete blood count (CBC) and in plain tubes for biochemical assay (activities of liver enzymes). The Blood pressure of subjects was measured directly after sample collection. Result: The blood pressure among the group of age 36-84y was significantly higher (P < 0.05) when compared between the smokers and the nonsmokers group, while among the group of age 15-35 was not significant. The results of liver enzymes activities among the group of age 36-84y showed that ALT and ALP were significantly high (P <0.05) in the smoker group when compared with the nonsmoker group, while serum AST was not significant (P>0.05). However, among the group of age between 15-35 years, the results showed that statistically significant differences (P<0.05) were observed in ALT and AST activities for the smoker group when compared with the nonsmoker group. Regarding RBCs count and hemoglobin concentration among both of groups (age between 15-35 & 36-84 years), the results showed that a significant difference in mean RBCs count and hemoglobin concentration were noted between the smokers and the nonsmokers. Conclusion: It can be concluded that exposure to cigarette smoking leads to an increase the blood pressure. Cigarette smoking can lead to an increase in liver enzymes activities, RBCs count and Hb concentration.

The liver is critical organ for metabolic homeostasis and toxic substance clearance and plays an important role in the systemic response to critical illness. Acute panreatitis (AP) progresses with a local production of inflammatory mediators, eventually leading to systemic inflammatory response syndrome. Knowing that almost all pancreatic mediators released from the pancreas to the blood stream may pass through the liver before their dilution in the systemic circulation, it would be reasonable to assume a determinant role of this organ in development of the inflammatory response associated with acute pancreatitis. Objectives: The study aimed to investigate the time courses of the effects of the exogenous glucocorticoids agonist dexamethasone on microscopical changes occurring in the liver of rats used as a model of AP induced by L-Arginine. Materials and Methods: 60 adult male albino rats weighing 150-200 gm were used. They were divided into 3 groups: Control group: Which is also divided into 2 subgroups (a & b) each of animals of the first were IM injected with 0.5ml/100gm B.W saline and those of second were injected by 0.5mg/100gm B.W dexamethasone. L-Arginine group: which received L-Arginine to induce AP. The animals of this group were divided into 3 subgroups a, b and c the animals of which were sacrificed 3 days, 2 weeks and 1 month after L-Arginine injection respectively. Dexamethasone and L-Arginine group: in which the animals were injected with both L-Arginine and dexamethasone. They were also divided into 3 subgroups a, b and c, the animals of which were sacrificed 3 days. 2 weeks, one month after the injection of the drugs. The liver of the scarified animals were dissected out and prepared for microscopical examination. Results: The histopathological changes that occurred in the livers of acute pancreatitis (AP) model animals started in the periphery of the classic hepatic lobules and progressively extended in a centripetal manner to involve all the cells of the lobules in the late period of the experiment. These changes were in the form of ballooning of the hepatocytes, progressive vacuolation of their cytoplasm most propably with fat globules and depletion of the PAS+ve glycogen granules. Injection of dexamethasone in AP model animals did not improve the case, but on the contrary it made the changes more intense, severe, and rapid. One month after injection of L-Arginine and dexamethasone, the hepatocytes all over the hepatic lobules were severely affected. They were markedly ballooned with severely vacuolated cytoplasm which was completely depleted from its PAS +ve glycogen granules, indicating severe fatty degeneration of the liver. Conclusion: From the previous data, it can be concluded that treatment of AP with dexamethasone is caused a late bad effect on the liver, where it causes its late fatty liver changes.

The therapeutic effect of Cyclophosphamide (CPA) is thus attributed to phosphoramide mustard and acrolein leads to the formation of high levels of reactive oxygen species (ROS), which results in decreased antioxidant activity. Excessive production of ROS could also culminate in oxidative stress. Objectives: This study aims to evaluate the effect of sub-lethal dose of the cyclophosphamide, 5-FU, combination of 5-FU, and CPA on testicular antioxidant status, and oxidative stress in male albino rats. Materials and Methods: Twenty-eight male adult rats were grouped randomly into four groups (n=5 each group). Group I (control): Rats were injected with saline intraperitoneally and at a dose of 1.0 ml/kg b.w. for 14 days. Group II cyclophosphamide (CPA): Cyclophosphamide at a dose of 10 mg/kg day by day through i.p. to rats for 14 days. Group III Fluorouracil (5-FU): 5-Fluorouracil at a dose of 10 mg/kg day by day in saline was given through i.p. to rats for 14 days. Group IV (CPA+5-FU): Rats were given CPA followed by 5-FU at a dose of 10 mg/kg per day (day by day) through i.p. to rats for 14 days. At the end of the experimental period, rats were anesthetized using light ether. Blood and testes tissue samples were taken and prepared for biochemical measurements. Biochemical parameters in rat serum and tissues were evaluated. Results: Individual injection of CPA and 5-FU to rats were reduced testes TAC, GSH concentration, GR, and CAT activities compared to control. However, the combination treatment of rats with 5-FU and CPA increased the levels of these non-enzymatic and enzymatic antioxidant compared with those treated with CPA alone. Also, results showed significantly increased TBARS and NO concentration in the testes of CPA treated rats when compared to normal ones, while 5-FU increased NO only compared with the control. Conclusion: It can be concluded that treatment of rats with CPA is associated with the production of free radicals that leads to hazardous alterations in certain non-enzymatic, and enzymatic functions. The increase in lipid peroxidation probably leads to the intracellular accumulation of ROS with the subsequent development of testes tissue injury. However, 5-FU and CPA combination could produce a significant amelioration in most cases for these changes, and it may be considered as a potentially useful candidate in the combination chemotherapy with CPA to combat oxidative stress mediated non target organs injury even if it was not a complete protection. Future work should consider combined chemotherapy regimens, as two or more mechanisms of action of chemotherapeutic drugs could be more powerful than one mechanism.

Background: Cyclophosphamide (CPA) induces acute inflammation of the urinary bladder, renal damage, and liver damage, thereby limiting its therapeutic use. Objectives: The present study aimed to evaluate the hepatorenal toxicity induced by cyclophosphamide and amelioration by 5-fluorouracil in male albino rats. Materials and Methods: Twenty-eight male adult rats were grouped randomly into four groups (n=5 for each group). Group I (control): Rats were injected with saline intraperitoneally and at a dose of 1.0 ml/kg b.w. for 14 days. Group II cyclophosphamide (CPA): Cyclophosphamide at a dose of 10 mg/kg day by day through i.p. to rats for 14 days. Group III Fluorouracil (5-FU): 5-Fluorouracil at a dose of 10 mg/kg day by day in saline was given through i.p. to rats for 14 days. Group IV (CPA+5-FU): Rats were given CPA followed by 5-FU at a dose of 10 mg/kg per day (day by day) through i.p. to rats for 14 days. At the end of the experimental period, rats were anesthetized using light ether. Blood samples were taken and prepared for biochemical measurements. Results: Serum total protein, albumin, and globulin concentration significantly reduced in animal groups that received cyclophosphamide. 5-FU and CPA combination reduced the changes in total protein, albumin, and globulin compared to CPA treated group. A significant increase in LDH serum concentration was found in CPA, 5-FU, and their combination-treated animals. The mean values of the combination of chemotherapy were above that in CPA followed by 5-FU treatment. Administration of CPA, 5-FU resulted in a significant increase in serum AST, ALT, ALP, and bilirubin compared to the control. Co-treatment 5-FU with CPA significantly attenuated the increase in serum AST, ALT, ALP, and bilirubin when compared to CPA – treated rats. Compared to controls, urea and creatinine levels were increased in CPA-treated rats, while uric acid was reduced in CPA, 5-FU, and their combination. The changes in urea and creatinine produced by the chemotherapy were restored when rats received CPA in combination with 5-FU. Conclusion: It could be concluded that the treatment of mammals with chemotherapy is associated with the production of free radicals that lead to hazardous alterations in biochemical parameters. However, 5-FU and CPA combination could produce a significant amelioration in most cases for these changes, and it may be considered as a potentially useful candidate in the combination chemotherapy with CPA to combat oxidative stress-mediated non-target organ injury even if it was not complete protection. Future work should consider combined chemotherapy regimens, as two or more mechanisms of action of chemotherapeutic drugs could be more powerful than one mechanism. Toxicological studies must be performed before using drugs as a combination before application. Further research is required on the toxicological impacts of drugs and pollutants mixtures.