Reproductive dysfunction is often characterized by malfunction of the reproductive tissues, which may lead to disruption of the synergistic rhythm that should bring about a progression of sexual events and the conception of new life. This may therefore result in the sexual dysfunction and infertility that can be seen in couples having prolonged biological difficulty in reproducing their offspring after having unrestricted sexual intercourse for at least twelve months. Several factors have been implicated in the cause and progression of reproductive dysfunction, including poor nutrition, drug side effects, disease states, and toxicant ingestion. A well-known food additive that has been found to be potent at initiating reproductive anomalies in males is monosodium glutamate (MSG). This regular flavor enhancer is widely used as a taste enhancer in several diets. The different mechanisms by which it may induce reproductive dysfunctions include spermatogenic alteration resulting in a low sperm count, high sperm abnormality, reduced live sperm and decreased sperm pH, oxidative damage (increased lipid peroxidation and reduced antioxidant enzyme activities), histological alteration (blood hemorrhage, distorted germ and Sertoli cells), as well as gonadotropin imbalance (reduced testosterone, luteinizing hormone, and follicle-stimulating hormone concentrations). Therefore, this review discusses various established mechanisms through which MSG may induce reproductive dysfunction and the treatment strategies to ameliorate its toxic effects.

Benign prostatic hyperplasia (BPH) is a urological disease characterized by proliferation of the stromal and epithelial cells of the prostate of older men. Ketogenic diet (KD) is a high fat, moderate protein and low carbohydrate diet which acts on metabolic systems through hormonal modulation and simulation amongst other mechanisms. This study investigated the effect of KD consumption in Testosterone Propionate (TP) induced BPH. Twenty-Five male rats were divided into five groups of five animals each; control and KD group were administered distilled water and KD respectively, while the remaining groups were given 30 mg/kg body weight of TP subcutaneously once daily for 28 days. Thereafter, the three groups, TP, TP + Finasteride, TP + KD were administered standard rat chow, finasteride (0.1 mg/kg) and KD respectively, for 42 days prior to sacrificing the rats and their serum and prostate glands obtained for analysis. Triglyceride, Total cholesterol, HMG CoA reductase, Follicle Stimulating Hormone, Luteinizing Hormones, Testosterone, Prostate Specific Antigen (PSA) concentration and Malondialdehyde levels were significantly increased (p ≤ 0.05) while superoxide dismutase, catalase and glutathione peroxidase activities were significantly (p ≤ 0.05) reduced in the TP group. These changes were reversed significantly (p ≤ 0.05) in the finasteride and KD treatment groups. The diet also caused significant (p ≤ 0.05) decrease in prostate weight and stromal glandular tissue. This study suggests that ketogenic diet consumption ameliorated prostatic hyperplasia in the rats and may be considered as an affordable and non-invasive management option for benign prostatic hyperplasia in men.