Brain structure is always the first dam against effect drug delivery to treatment of neurologic disorders. Oxidative stress is a critical condition in the pathogenesis of neurologic disorders. N-acetylcysteine amide(NACA), a lipophilic derives of N-acetylcysteine (NAC) that showed a great potential to treatment of oxidative based disorder especially in the brain. we evaluated 83 publications whose title contain NACA. Cast a glance on all the document which showed NACA has protective effect on toxins-drugs toxicity. Most of the articles reported that NACA is a great therapeutic option for cataracts and eye disorders. Hematologic problem and kidney related disorders is a target for NACA. Then, we focused on the neurological application of NACA. It is well-documented that the bio effects of NACA is mediated by antioxidant properties via –SH group. It is more bioavailable and potent than NAC. is significantly higher than NAC. The lipophilic structure confers promising effect to NACA for brain disorders treatment range from trauma to toxins and neurotransmitter toxicity. Manuscript profile

Betaine, a multifunction molecule, has a cardio protective feature but the mechanism is not well-understood. Hence, we evaluated the effect of betaine on cardiac tissue and serum biomarkers. Betaine administered to Albino rats at 50, 150 and 250 mg/kg, and sham group received deionized water. Myocardial infarction was induced by isoproterenol (100 mg/kg). The tunnel test and immunohistochemistry were performed on heart tissue to detect apoptosis and nitric oxide levels respectively. Serum levels of lipid peroxidation (LPO) and superoxide dismutase (SOD) were measured with colorimetric methods. The apoE and Bcl-2 gene expression were measured by RT-PCR in heart tissues and peripheral blood mononuclear cells (PBMCs). The results showed that betaine pretreatment at 250mg/kg for 60 days which reduces the apoptotic cells in the heart tissue after isoproterenol-induced myocardial infraction (P= 0.038). Cardiac Bcl-2 levels were upregulated by betaine, in which the maximum levels were observed in 150 mg/kg dosage. Similar finding was observed in the apoE expression in PBMCs. The tissue NOS levels were not change by betaine pretreatment significantly. Both superoxide dismutase and lipid peroxidation levels were reduced by betaine pretreatment dose dependently. Our results confirm the protective effect of betaine pretreatment that is mediated by Bcl-2 and anti-oxidative properties. Manuscript profile