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BackgroundParacetamol is one of the widely used antipyretic and analgesic drug around the world. Many researchers showed that paracetamol caused to hepatotoxicity or nephrotoxicity.ObjectiveIn the present study, we aimed to determine whether betaine has protective effects on hepatotoxicity and nephrotoxicity in neonate rats, following to long term maternal paracetamol exposure.Materials and methodsRandomly chosen neonates, from the neonate pools, were divided into three groups; Control (n=13), APAP (n=13), and APAP+Betaine (n=13). Physiological saline, paracetamol (30 mg/kg/day), and paracetamol (30 mg/kg/day)+betaine (800 mg/kg/day) were orally administered to the relevant groups during the pregnancy period (approximately 21 day). Following to the birth, neonates were decapitated under anaesthesia and tissue samples were taken for biochemical and histological analyses.ResultsThe statistical analysis showed that, malondialdehyde and nitric oxide levels increase significantly in APAP group, while paraoxonase, arylesterase activity and glutathione levels decrease. After the betaine administration, glutathione levels, paraoxonase and arylesterase activities increased while malondialdehyde and nitric oxide levels decreased in APAP+betaine group. These biochemical findings also were supported by histological results.ConclusionIn this study, our biochemical and histological findings indicate that betaine can protect the tissue injury caused by paracetamol.

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AIM: Oxidative stress (OS) and lipid peroxidation (LP) occur in a cell due to irreversible damage resulting from incidents such as traumatic brain injury (TBI). The aim of our study was to investigate the possible neuroprotective effect of boric acid (BA) by examining the changes in catalase (CAT) activity and levels of CAT and malondialdehyde (MDA) in brain tissues from rats with closed head trauma. MATERIAL and METHODS:The study consisted of three groups: control ,TBI and TBI + BA. Animals in the control and TBI groups received saline, while animals in the TBI + BA group received BA through daily oral gavage, for 14 days prior to TBI was performed using the modified Marmarou impact acceleration model. After 24 hours,animals were euthanized and brain tissue obtained to measure the levels of MDA and to assess the activity of CAT. RESULTS: MDA levels and CAT activity were significantly higher in the TBI group versus the control group. However, they were significantly lower in the TBI + BA group compared to TBI alone. Similarly, edema and necrotic neurons were observed in the TBI group, but not in the control or TBI + BA groups. CONCLUSION:Based on biochemical and histopathological evidence, we determined that TBI induced LP and OS were inhibited by pre-treatment with BA.