Peganum harmala L. extract reduces oxidative stress and improves symptoms in 6-hydroxydopamine-induced Parkinson's disease in rats

Parkinson's disease is one of the most common neurodegenerative disorders. There are many documents about the effects of oxidative stress in Parkinson's disease etiology. Angiotensin II activates NADPH dependent oxidases and causes superoxides formation. Peganum harmala L. extract, which has angiotensin converting enzyme [ACE] inhibitory effect, is considered to evaluate oxidative stress inhibition and Parkinson's disease improvement. Male rats weighting 200-250 g were divided into 5 groups: Control, Neurotoxin [injection of 6-hydroxydopamine into left hemisphere substantia nigra], Peganum harmala's seedsaqueous extract [10 mg/kg] and captopril [5 mg/kg]. Peganum harmala and captopril were injected intraperitonealy -144, -120, -96, -72, -48, -24, -2, 4 and 24 h relative to 6-hydroxydopamine injection time. Muscle stiffness, apomorphine induced unilateral rotation, amount of brain's protein oxidation and lipid peroxidation, ACE activity and histology of substantia nigra were assayed in all groups. Peganum harmala improved Muscle stiffness and one-direction rotation behavior significantly. It also reduced brain's lipid and protein oxidation levels in neurotoxin-injected rats significantly. In Peganum harmala group compared to control group, brain's ACE activity was significantly inhibited. In histological study, Peganum harmala prevented degeneration of dopaminergic neurons, too. In conclusion, aqueous extract of Peganum harmala could prevent symptoms and reduced oxidative stress markers in rats with Parkinson's disease induced by 6-hydroxydopamine

[Study of the therapeutic effect of melatonin after food deprivation in apoptosis and oxidative stress in rat testis]

The goals of the study are evaluation the effect[s] of food deprivation as a social stress on testis structure. We also investigated the effects of melatonin treatment as an antioxidant component and inequality on the effect[s] of food deprivation. We investigated the improving effects of melatonin and social stress [food deprivation] on 42 male rats in 7 groups including control, sham, melatonin received [M], food deprivation [1/3 of control daily food] plus observation [FD], FD + melatonin [FDM], isolated FD [FDi], and FDi + melatonin [FDMi] groups. After 14 days, rats' testes were studied using immuno histochemistry and TUNEL assays to determine the number of apoptotic cells. Biochemical evaluation was taken on malodialdehide [MDA] and glutathione [GSH]. ANOVA and Tukey's tests were done to analyse the data. P<0.05 was considered statistically significant. The results of sham group was declined for similarity to results of control group. In FD group, MDA was increased significantly [P<0.01], GSH was decreased and the number of apoptotic cells was increased, significantly [P<0.01]. In FDi group, there was no effect on the ratio of oxidative stress compared to the control group. Melatonin treatment could decrease apoptotic cells [P<0.05] and MDA concentration [P<0.05] in the FD group. Food deprivation can induce oxidative stress which is associated with increasment of apoptotic cells in testis. Isolation can compensate these effects. These results refer to inequality. Since melatonin is recognized for its anti-oxidative and improving effects, we have shown involvement of oxidative stress mechanisms on the stress of food deprivation with inequality