Plant-derived compounds have recently attracted greater interest in the field of new therapeutic agent development. These compounds have been widely screened for their pharmacological effects. Polyphenols, such as soy-derived isoflavones, also called phytoestrogens, have been extensively studied due to their ability to inhibit carcinogenesis. These compounds are chemically similar to 17β-estradiol, and mimic the binding of estrogens to its receptors, exerting estrogenic effects in target organs. Genistein is an isoflavone derived from soy-rich products and accounts for about 60% of total isoflavones found in soybeans. Genistein has been reported to exhibit several biological effects, such as anti-tumor activity (inhibition of cell proliferation, regulation of the cell cycle, induction of apoptosis), improvement of glucose metabolism, impairment of angiogenesis in both hormone-related and hormone-unrelated cancer cells, reduction of peri-menopausal and postmenopausal hot flashes, and modulation of antioxidant effects. Additionally, epidemiological and clinical studies have reported health benefits of genistein in many chronic diseases, such as cardiovascular disease, diabetes, and osteoporosis, and aid in the amelioration of typical menopausal symptoms, such as anxiety and depression. Although the biological effects are promising, certain limitations, such as low bioavailability, biological estrogenic activity, and effects on target organs, have limited the clinical applications of genistein to some extent. Moreover, studies report that modification of its molecular structure may eliminate the biological estrogenic activity and its effects on target organs. In this review, we summarize the potential benefits of genistein on menopause symptoms and menopause-related diseases like cardiovascular, osteoporosis, obesity, diabetes, anxiety, depression, and breast cancer.

The administration of a relatively high dose of antidepressant drugs produces an increased neuronal firing rate of the lateral septal nucleus (LSN) in the rat and a decreased immobility in rats forced to swim. However, it is unknown whether a minimally effective low-dose 21-day treatment with the selective serotonin reuptake inhibitor, fluoxetine, while reducing immobility in the forced swim test, also increases the neuronal firing rate of the LSN in Wistar rats. The total time of immobility decreased with a daily injection of 0.5, 1.0 or 2.0 mg/kg of fluoxetine (p< 0.001), and the lowest dose increasing the latency to the first immobility period (p < 0.0001) was 1.0 mg/kg. Therefore, the action of the 21-day fluoxetine treatment (1.0 mg/kg) on the firing rate of LSN neurones was tested in another group of rats. A total amount of 78 single-unit extracellular recordings was taken from the LSN of eight control rats (n = 40) and eight fluoxetine treated rats (n = 38). The LSN firing rate in the fluoxetine group was double (18.3 ± 2.5 spikes per 10 s, p< 0.05) that in the control group (7.0 ± 0.9 spikes per 10 s), and the first order interval of firing proved to be significantly lower in the fluoxetine group compared to the control group (384.3 ± 22.3 and 639.7 ± 27.5 ms, respectively; p < 0.05). In conclusion, the increased neuronal firing rate of the LSN in the animals treated with a low dose of fluoxetine may be associated with an increased motivation to escape from the stressful situation that the forced swim represents.

A mixture of eight fatty acids (linoleic, palmitic, stearic, myristic, elaidic, lauric, oleic, and palmitoleic acids) at similar concentrations identified in human amniotic fluid produces anxiolytic-like effects comparable to diazepam in Wistar rats. However, individual effects of each fatty acid remain unexplored. In Wistar rats, we evaluated the separate action of each fatty acid at the corresponding concentrations previously found in human amniotic fluid on anxiety-like behaviour. Individual effects were compared with vehicle, an artificial mixture of the same eight fatty acids, and a reference anxiolytic drug (diazepam, 2 mg/kg). Myristic acid, the fatty acid mixture, and diazepam increased the time spent in the open arms of the elevated plus maze and reduced the anxiety index compared with vehicle, without altering general locomotor activity. The other fatty acids had no effect on anxiety-like behaviour, but oleic acid reduced locomotor activity. Additionally, myristic acid produced anxiolytic-like effects only when the concentration corresponded to the one identified in human amniotic fluid (30 ????g/mL) but did not alter locomotor activity. We conclude that of the eight fatty acids contained in the fatty acid mixture, only myristic acid produces anxiolytic-like effects when administered individually at a similar concentration detected in human amniotic fluid.

Acrylamide is a vinyl monomer that is widely used for the synthesis of polyacrylamides, the treatment of drinking water, and as an additive in cosmetics. Acrylamide is also produced during the thermal processing of carbohydrate-rich foods. Although the potential toxic effects of acrylamide have been reported, few studies have evaluated biochemical parameters in blood. The present study investigated alterations of blood chemistry, hepatic function, and blood cytometry in acrylamide-treated rats. Thirty-two male Wistar rats were assigned to four experimental groups (n = 8/group): one control group received 0.3 ml of vehicle (saline solution), and the other three groups received acrylamide (25, 50, and 75 mg/kg, i.p., for 14 days). At the end of treatment, blood samples were collected to obtain serum, which was then processed using a Vitros250 device. For blood cytometry, the samples were processed in a Sysmex analyzer. The blood chemistry results showed that urea nitrogen, urea, and creatinine were elevated in the acrylamide-treated groups. Tests of hepatic function showed that total and direct bilirubins, transaminases, and alkaline phosphatase were also elevated compared with vehicle, whereas the levels of total proteins and albumin decreased. Blood cytometry showed that the levels of erythrocytes, hemoglobin, hematocrit, leukocytes, and platelets and mean cell volume decreased in the acrylamide-treated groups compared with vehicle. Overall, the present findings indicate that acrylamide causes deleterious effects on renal and hepatic physiology, producing dose-dependent alterations of blood chemistry and cytometry parameters in male Wistar rats.