The rising occurrences of male reproductive disorders, as decreased semen (quality and quantity) and testicular cancer, are of great concern for animal production. Therefore, this study was conducted to determine the toxic impact of cypermethrin on the fertility of male rats. Other goal was using the Panax ginseng as androgenic drug for reducing the negative impact of cypermethrin poisoned rats. In the results, oral LD50 of cypermethrin in mature male rats was found to be 374.633 ±12.187 mg/kg. Based on that, thirty-two adult male rats were equally divided into four groups. Group (1) served as –ve control; group (2) treated with 0.1% Panax in feed and kept as +ve control; group (3) orally dosed 1/40 LD50 of cypermethrin; and group (4) intubated the same dose of cypermethrin and panax admixed with diet for 60 days. The results demonstrated that cypermethrin generated obvious disorders in male fertility as evidenced by a significant decrease in the blood testosterone, LH and FSH hormones, testes weights, sperm count and motility, and live sperm percentage. Sperm cell abnormalities were significantly elevated in cypermethrin poisoned rats compared. Although the group treated by cypermethrin with panax showed a lesser effect. Cypermethrin intoxication showed sever alteration in fertility indices and fetal values. Histopathological examinations on the testes, seminal vesicles, and prostate glands served as confirmation for all findings. A positive control group didn’t significantly differ as compared to a negative control. Otherwise, it recorded the best results in percentage of motile and live sperm, especially drops of sperm cell abnormalities. Results concluded that involvement with cypermethrin caused overt defects in male reproductive function, which were cured by administering the androgenic drug Panax.

The modulatory effects of Panax ginseng on the pancreatic β-cell activity, glucose metabolism and its hepatoprotective action in alloxan induced - type 2 diabetic male rats were studied for 2 months. We divided the rats randomly into six equal groups; control; diabetic (T2DM); ginseng,  ginseng post T2DM induction; ginseng pre T2DM induction and ginseng pre and post T2DM induction. The serum level of glucose, total cholesterol (TC), high-density lipoprotein (HDL), low-density lipoprotein (LDL), very low-density lipoprotein (VLDL),  triglycerides (TG), total protein, albumin, globulin, albumin- globulin ratio (A/G), total bilirubin, both  direct and indirect  bilirubins,  gamma glutamyl transferase (GGT), alanine aminotransferase (ALT), aspartate aminotransferase (AST), cytochrome P450 (CYP450) and the activity of hepatic glucose -6- phosphatase (G6Pase) and also, the activity of the antioxidant markers [glutathione peroxidase (Gpx), catalase (CAT), superoxide dismutase (SOD), in addition; the level of lipid peroxidation product; malondialdehyde (MDA)] in both  the serum and the liver were measured. The histological structure of both the pancreas and the liver and the expressions of both insulin receptors (IR), adenosine monophosphate kinase (AMPK) and the percentage  of the positive area of insulin secretion in the islets of Langerhans using immunohistochemistry technique were also estimated.  The results revealed that the previously mentioned parameters were significantly improved after administration of Panax ginseng to diabetic rats. In conclusion panax ginseng administration could be ameliorate and protect the male rats against type 2 DM and could be able to decrease the intensity of damage caused in the pancreas after alloxan injection.

The effects of red ginseng and raw ginseng were examined in vivo mid-term test for hepatocarcinogens in rats. The number of placental type of glutathione S-transferase (GST-P)-positive foci of the liver was significantly reduced in rats given diethylnitrosamine (DEN) followed by raw ginseng (4.77 +- 3.23, p0.05) as compared to the controls given carcinogen alone (9.07 +- 5.69). The area of GST-P positive foci was also significantly reduced in rats given DEN followed by red ginseng (0.5 +- 0.31, p0.05) as compared to the control (0.93 +- 0.65). These result suggest that red or raw ginseng are not hepatocarcinogens and rather may possess inhibitory potential for liver carcinogenesis