Recently, there is growing interest in the natural bioactive components having anticancer activity. Thymoquinone (TQ), the principle active constituent of black seed (Nigella sativa), has promising properties including anticancer and chemosensitizing peculiarities. The anticancer power of TQ is accomplished by several aspects; including promotion of apoptosis, arrest of cell cycle and ROS generation. In addition, it boosts the immune system and lessens the side effects associated with traditional anticancer therapy. TQ also controls angiogenesis and cancer metastasis. This review focuses on the potential aspects and mechanisms by which TQ acquires its actions.

The aim of this study was to investigate the protective effects of cinnamon on lead acetate induced reproductive toxicities in rats. Thirty-two male rats were randomly divided into 4 groups, 8 rats in each. Control rats received distilled water, while treated rats received lead acetate (30 mg/kg), cinnamon (250 mg/kg) and lead acetate and cinnamon (30 mg/kg and 250 mg/kg) for 60 days by gavage tube. In cinnamon treated rats, the relative weights of testes, epididymis, seminal and prostate glands were significantly (P < 0.05) increased compared with that in lead acetate treated rats. Sperm cell concentration and viability were significantly (P < 0.05) reduced, while sperm abnormalities were significantly (P < 0.05) increased in lead treated rats. The superoxide dismutase (SOD) and catalase activities were significantly reduced (P < 0.001) in lead acetate treated rats compared to the other groups, while the addition of cinnamon to lead acetate improved the level of SOD compared to the lead treated group. There was a marked reduction (P < 0.001) in the expression of androgen receptor and significant (P < 0.001) increase in the level of caspase-3 protein expression in the testis of lead treated rats. In conclusion, cinnamon exhibited protective effect on reproductive system by inhibiting lead acetate induced oxidative stress and excessive cell apoptosis.

Diabetes mellitus is one of the metabolic diseases having several complications.Nigella sativaoil (NSO) might have beneficial effects in the treatment of diabetic complications. Thirty‐two mature male Wistar rats were equally divided into four experimental groups: control, control NSO 2 mL/kg, streptozotocin‐ (STZ‐) induced diabetic, and diabetic (STZ‐induced) treated with oral NSO 2 mg/kg for 30 days. Fasting blood glucose (FBG), insulin, and lipid profile levels were determined. Pancreatic and hepatic tissues were used for catalase and GSH. Histopathology, hepatic glycogen contents, insulin immunohistochemistry, and pancreatic islet morphometry were performed. NSO 2 mL/kg was noticed to decrease (P< 0.05) FBG and increase (P< 0.05) insulin levels in diabetic rats than in diabetic nontreated animals. Lipid profile showed significant (P< 0.5) improvement in diabetic rats that received NSO 2 mL/kg than in the diabetic group. Both pancreatic and hepatic catalase and GSH activities revealed a significant (P< 0.05) increment in the diabetic group treated with NSO than in the diabetic animals. NSO improved the histopathological picture and hepatic glycogen contents of the diabetic group as well as increased (P< 0.05) insulin immunoreactive parts % and mean pancreatic islet diameter. NSO exerts ameliorative and therapeutic effects on the STZ‐induced diabetic male Wistar rats.

Bisphenol A (BPA)—an endocrine disruptor xenoestrogen—is widely spread in the environment. Lycopene (LYC) is an antioxidant phytochemical carotenoid. The hereby study was designed to verify the deleterious effect of BPA on cyclic female rats’ hepatic tissue as well as evaluation of the effect of LYC toward BPA hepatic perturbation. Twenty‐eight female Wistar rats were allocated equally into four groups: control group, LYC group (10 mg/kg B.wt), BPA group (10 mg/kg B.wt), and BPA + LYC group (the same doses as former groups). The treatments were given daily via gavage to the rats for 30 days. The rats in BPA displayed high activities of serum liver enzymes with low levels of total proteins (TP) and albumin. Moreover, BPA induced hepatic oxidative stress via depletion of antioxidant enzymes concomitant with augmentation of lipid peroxidation, increased comet tail DNA %, and overexpression of caspase‐3. Meanwhile, LYC administration reduced the cytotoxic effects of BPA on hepatic tissue, through improving the liver function biomarkers and oxidant‐antioxidant state as well as DNA damage around the control values. These findings were confirmed by hepatic histopathological examination. Finally, LYC credited to have a noticeable protective effect versus BPA provoked oxidative injury and apoptosis of the liver tissue.

Keeping in mind the beneficial effects of GTE administration on liver damage, the present study was undertaken to evaluate the hepatoprotective effect of green tea extract (GTE) against carbon tetrachloride (CCl4)-induced liver injuries in male hamsters for 8 weeks. Twenty hamsters were equally divided into 4 groups, the control ones (group I) received only dis. water. Hamsters of group II had free access to 10% of GTE, while hamsters of group III received 1 ml/kg of 50% CCl4 in corn oil via gavage daily. Hamsters of group IV (GTE + CCl4) received a free access to GTE supplementation in combination with 1 ml/kg of 50% CCl4 in corn oil via gavage daily. Lipid profile, hepatic enzyme levels and apoptosis molecular marker (p53) were investigated in hamsters. GTE + CCl4 treated hamsters showed lower levels of hepatic malondialdehyde (MDA) than CCl4 exposed hamsters. Hepatic activity levels of GSH, ALD and cytochrome 450 reductase were declined after CCl4 administration while they were remarkably improved with GTE administration. Serum lipid profiles as T-cholesterol (TC), triglyceride (TG) and low density lipoproteins (LDL) were improved in GTE and CCl4 treated hamsters than CCl4 group. Moreover, hepatic tissue damage and p53 expression induced with CCl4 were improved with the treatment of GTE. These results suggested that GTE possesses hepatoprotective properties against the effect of CCl4.