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Omega-3 is a polyunsaturated fatty acid known to have immunomodulatory functions. In the present study, ameliorative potential of omega-3 in experimental carbon tetrachloride (CCl4) toxicity was investigated. Total of 40 adult male Wistar albino rats were allocated into five groups and were subcutaneously given once every two days for 6 weeks the followings: Group 1 (Control): 0.5 ml/kg serum physiologic, Group 2 (Omega): 0.5 g/kg omega-3, Group 3 (Vehicle): 0.5 ml/kg pure olive oil, Group 4 (CCl4): 0.5 ml/kg CCl4, Group 5 (CCl4 + Omega): 0.5 ml/kg CCl4 plus 0.5 g/kg omega-3. At the end of the treatments, blood samples were collected and necropsy was performed for collection of liver tissues. Serum AST, ALT, GGT, TAC, TOC, triglyceride, and visfatin levels were detected. Liver morphology and immunoreactivities against TGF-α, TGF-β, PPAR-α, and PPAR-γ were assessed. Serum AST, ALT, GGT, and TOC levels significantly increased while TAC level decreased in CCl4 given animals as compared to the control group. No significant changes were observed in triglyceride and visfatin levels. Immunohistochemical staining revealed increased TGF-α and TGF-β expressions and decreased PPAR-α and PPAR-γ expressions in liver of CCl4 given animals. Omega-3 supplementation has prominent effects in correcting the biochemical and immunohistochemical parameters studied as well as the tissue morphology. The results of the investigation indicated that omega-3 has ameliorative effects on the oxidative tissue degeneration and inflammatory processes induced by CCl4 treatment in rats

Venlafaxine is the first antidepressant that acts via inhibiting serotonin and noradrenaline reuptake. Hypertension is observed in doses exceeding 300 mg/day and is the most feared complication. We report a patient with accelerated hypertension after venlafaxine use observed at a dose of 150 mg/day. A 23-year-old patient with symptoms of insomnia, depression, anhedonia, fatigue admitted our clinic. Venlafaxine at a dose of 75 mg/day was initiated after he was diagnosed with major depressive disorder. After 5 months, venlafaxine dose was uptitrated to 150 mg/day due to inadequate response to drug. After using venlafaxine for ten months at the dose of 150 mg/day, he admitted our clinic with headache and epistaxis. He was hospitalized after his blood pressure was measured as 210/170 mmHg. No secondary causes for hypertension were found, and venlafaxine treatment was considered possible etiologic factor. After stopping venlafaxine treatment, his blood pressure was reverted back to normal limits. While mild elevation of blood pressure could be observed after venlafaxine treatment, this case shows that accelerated hypertension with a diastolic blood pressure rise above 120 mmHg could be observed at relatively low doses of venlafaxine. Close monitoring of blood pressure is necessary after initiation of treatment, as accelerated hypertension could cause endorgan damage with potentially catastrophic results.