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Valproic acid (VPA) is a broad-spectrum anticonvulsant drug. Its mechanism of action includes enhancing GABAergic transmission, blocking voltage-gated sodium channels, and affecting dopaminergic and serotonergic transmission (1). The mechanism of VPA toxicity, including its effects on the liver, is not fully known. It is assumed that oxidative stress and/or reactive products of drug biotransformation are responsible for its hepatotoxicity (2). The aim of the study was to verify the hypothesis concerning the influence of valproic acid and its metabolite, 2-propyl-4-pentenoic acid (4-en VPA) on the antioxidant status of patients treated with (VPA-T) and poisoned with valproic acid (VPA-P). The VPA-P group was divided into patients with (VPA-Ptox) and without (VPA-Pnon) toxic symptoms observed during the hospitalization. Oxidative stress was assessed using markers, such as antioxidant potential (FRAP) and reduced and oxidised glutathione (GSH/GSSG) ratio were measured in the plasma of the study patients. The obtained results showed statistically significant differences between the concentrations of the drug and its active metabolite levels in the VPA-T and VPA-P groups. In the VPA-P group, the increase of the level of 4-en VPA in the plasma correlated with the increase of the concentration of the drug. The influence of VPA on the antioxidant balance in both groups of patients was demonstrated. The plasma antioxidant potential of FRAP decreased with increasing valproic acid concentrations in the VPA-Ptox group. The lowest concentrations of GSH/GSSG ratio were found in the VPA-Pnon group, without symptoms of intoxication during hospitalization.

Quetiapine (QT) belongs to the second generation of antipsychotics. It is mostly used to treat depression, bipolar disorder, and schizophrenia. During biotransformation via myeloperoxidase (MPO) QT is oxidized to quinoneimine and a reactive radical, which may contribute to the development of oxidative stress during intoxication. The coexisting inflammation may also significantly contribute to the disturbances in the course of QT poisoning. In this study, twenty-one patients poisoned with quetiapine were examined. The study aimed to assess the correlation between blood QT concentration and selected oxidative stress as well as inflammation biomarkers, such as MPO and C-reactive protein (CRP) levels in the serum of poisoned patients. The obtained results were related to the values of the control group consisting of 21 healthy people, untreated and not poisoned with the drug. In patients with a toxic QT concentration in the blood (3.15 ± 2.11 μg/mL), the activity of MPO and CRP serum level were significantly higher in comparison to the control group. The mean level of CRP in the study group was 76.74 mg/L, while in the control group only 1.86 mg/L. The increase in MPO activity and CRP blood level in patients after QT overdose may confirm the hypothesis of oxidative disorders arising during its biotransformation and concomitant inflammation. Statistically significant relationships between selected biomarkers and blood QT concentration, the patient's clinical condition and the type of therapy were demonstrated.