The protective effect of vitamin E on locus coeruleus in early model of Parkinson's disease in rat: immunoreactivity evidence.

BACKGROUND: Free radical formation and oxidative stress might play an important role in the pathogenesis of Parkinson's disease (PD). In vitro data indicate that neuromelanin (NM) pigment is formed the excess cytosolic catecholamine that is not accumulated into synaptic vesicles via the vesicular monoamine transporter 2 (VMAT2). We designed this study to investigate the neuroprotective effects of vitamin E in the early model of PD. METHODS: Male rats (n = 40) with unbiased rotational behavior were randomly divided into five groups: sham operated group (SH, n = 8), vehicle-treated SH group (SH + V, n = 8), vitamin E-treated SH group (SH + E, n = 8), vehicle-treated lesion group (L + V, n = 8) and vitamin E-treated lesion group (L + E, n = 8). Unilateral intrastriatal 6-hydroxydopamine (12.5 microl) lesioned rats were treated intramuscularly with alpha-tocopherol acid succinate (24 I.U/kg, intramuscular [i.m.]) 1 h before surgery and three times per week for 2 month post-surgery. To evaluate the vitamin E pretreatment efficacy, tyrosine hydroxylase (TH) immunoreactivity and immunostaining intensity (ISI) for monoamine transporter 2 were used. RESULTS: TH immunohistochemical analyses showed a reduction of 20 percent in locus coeruleus (LC) cell number of vitamin E pretreated lesioned group but the cell number dropped to 60 percent in the lesioned group. The ISI of the cells was measured for VMAT2 in LC. Lesioned groups: 1) had the lowest VMAT2 ISI of all neurons; 2) There was an inverse relationship between VMAT2 ISI and NM pigment in the locus and 3) Neurons with the highest VMAT2 ISI also had high TH ISI. CONCLUSION: The data support the hypothesis that repeated i.m. administration of vitamin E exerts a protective effect on the LC neurons in the early model of PD.

Supplementation of freezing and thawing media with brain-derived neurotrophic factor protects human sperm from freeze-thaw-induced damage.

OBJECTIVE: To investigate the effects of brain-derived neurotrophic factor (BDNF) supplementation to freezing and thawing media on frozen-thawed human sperm parameters. DESIGN: Laboratory study. SETTING: University hospital. PATIENT(S): Semen samples from 21 healthy fertile men. INTERVENTION(S): We measured reactive oxygen species (ROS) by flow cytometry using the probes dichlorofluorescin diacetate for intracellular hydrogen peroxide (H2O2) and dihydroethidium for intracellular superoxide anion (O2-•), sperm plasma membrane integrity by flow cytometry, caspase-3 activity using ELISA, and AKT phosphorylation status using Western blot in sperm that was cryopreserved and thawed in media either supplemented with BDNF or without BDNF supplementation (control). MAIN OUTCOME MEASURE(S): Sperm motility, viability, ROS levels, caspase-3 activity and AKT phosphorylation. RESULT(S): The percentage of motile and viable sperm cells was significantly higher in BDNF-supplemented groups as compared with the nonsupplemented (control) group. There was a significant difference in AKT phosphorylation status between BDNF-supplemented groups and the control group. Moreover, the levels of intracellular H2O2 and caspase-3 activity were significantly lower in the sperm cells that were frozen and thawed in media supplemented with BDNF compared with in the control group. CONCLUSION(S): BDNF supplementation to sperm freezing or thawing media has protective effects against oxidative stress and apoptosis in frozen-thawed human spermatozoa and could improve sperm function, probably through the activation of AKT.