Thyroid dysfunction and diabetes are reported to be associated with depression. However, their role in the suicide risk in patients with major depressive disorder (MDD) is unclear. The purpose of this study was to investigate and compare thyroid dysfunction and diabetes between suicide attempters and non-suicide attempters in a large sample of first-episode drug-naïve (FEND) MDD patients. A descriptive study was conducted on 1279 Chinese outpatients with a diagnosis of first-episode MDD. Their sociodemographic information, blood levels of thyroid hormones, glucose, lipids and body mass index (BMI) parameters were collected. The positive subscales of the positive and negative syndrome scale (PANSS), Hamilton Anxiety Rating Scale (HAMA), Hamilton Depression Rating Scale (HAMD) were measured for psychotic, anxiety and depressive symptoms. Our results showed that compared with non-suicide attempters (P<0.01), suicide attempters had statistically higher scores on HAMD, HAMA and PANSS psychotic symptoms, as well as higher thyroid stimulating hormone (TSH) serum levels, glucose, anti-thyroglobulin (A-TG), anti-thyroid peroxidase (A-TPO), total cholesterol (TC), triglycerides (TG), low density lipoprotein cholesterol (LDL-C), systolic blood pressure and diastolic blood pressure (all with P<0.001). Further logistic regression analysis indicated that suicide attempts were associated with MDD. These results revealed that TSH, A-TG, A-TPO, TC, TG and LDL-C may be promising biomarkers of suicide risk in MDD, implying the importance of regular assessment of blood glucose level and thyroid function parameters for suicide prevention, along with possible treatment for impaired thyroid function and diabetes for the suicide intervention in MDD patients. Such patients with abnormal blood sugar and TSH must undergo thorough screening for suicidal ideation.

Brain cancer is regarded among the deadliest forms of cancer worldwide. The distinct tumor microenvironment and inherent characteristics of brain tumor cells virtually render them resistant to the majority of conventional and advanced therapies. Oxidative stress (OS) is a key disruptor of normal brain homeostasis and is involved in carcinogenesis of different forms of brain cancers. Thus, antioxidants may inhibit tumorigenesis by preventing OS induced by various oncogenic factors. Antioxidants are hypothesized to inhibit cancer initiation by endorsing DNA repair and suppressing cancer progression by creating an energy crisis for preneoplastic cells, resulting in antiproliferative effects. These effects are referred to as chemopreventive effects mediated by an antioxidant mechanism. In addition, antioxidants minimize chemotherapy-induced nonspecific organ toxicity and prolong survival. Antioxidants also support the prooxidant chemistry that demonstrate chemotherapeutic potential, particularly at high or pharmacological doses and trigger OS by promoting free radical production, which is essential for activating cell death pathways. A growing body of evidence also revealed the roles of exogenous antioxidants as adjuvants and their ability to reverse chemoresistance. In this review, we explain the influences of different exogenous and endogenous antioxidants on brain cancers with reference to their chemopreventive and chemotherapeutic roles. The role of antioxidants on metabolic reprogramming and their influence on downstream signaling events induced by tumor suppressor gene mutations are critically discussed. Finally, the review hypothesized that both pro- and antioxidant roles are involved in the anticancer mechanisms of the antioxidant molecules by killing neoplastic cells and inhibiting tumor recurrence followed by conventional cancer treatments. The requirements of pro- and antioxidant effects of exogenous antioxidants in brain tumor treatment under different conditions are critically discussed along with the reasons behind the conflicting outcomes in different reports. Finally, we also mention the influencing factors that regulate the pharmacology of the exogenous antioxidants in brain cancer treatment. In conclusion, to achieve consistent clinical outcomes with antioxidant treatments in brain cancers, rigorous mechanistic studies are required with respect to the types, forms, and stages of brain tumors. The concomitant treatment regimens also need adequate consideration.

Objective. Oxidative stress factors and proinflammatory cytokines had been found to be involved in the pathogenesis of patients with tardive dyskinesia (TD). This study assumes that blood biochemical markers would have a link with TD in schizophrenia patients. To explore the correlation between blood biochemical markers and tardive dyskinesia in patients with schizophrenia (SCH). Methods. From January 2010 to August 2021, the inpatients who met the diagnostic criteria of schizophrenia in the Chinese Classification and Diagnosis Criteria of Mental Disorders (DSM-4) and the American Diagnostic and Statistical Manual of Mental Disorders (DSM-4) were followed up in the psychiatric outpatient department of Jinxia Street Community Health Service Center, Longhu District, Shantou City. The diagnostic criteria of Abnormal Involuntary Movement Scale (AIMS) used in the TD study of Schooler and Kane were used to screen the patients. Patients were divided into the schizophrenia (SCH group) and the schizophrenia with TD groups (TD group). Oxidative stress factors including Superoxide Dismutase1 (SOD1), Glutathione Peroxidase1 (GPX1), Malondialdehyde1 (MDA1), Catalase Activity1 (CAT1), and brain-derived neurotrophic factor 1 (BDNF1) and some inflammatory cytokines including interleukin-2 (IL-2), interleukin-6 (IL-6), interleukin-8 (IL-8), serum tumor necrosis factor (TNF-α), prolactin, estrogen, and cortisol were measured in 121 schizophrenic patients with tardive dyskinesia and 118 schizophrenic patients. The correlation analysis was conducted on the data. Results. Age and female were immutable risk factors for the development of TD, and there were significant differences in blood biochemical indices GPX1, MDA1, CAT1, and TNF-α in schizophrenic patients with and without TD. Conclusion. This study supports that oxidative stress and immune disorders are associated with TD patients. Blood biochemical markers GPX1, MDA1, CAT1, and TNF-α may play an important role in the pathogenesis of schizophrenia combined with TD patients, and they may be useful in the diagnosis of schizophrenia with tardive dyskinesia.