Comparison of melamine exposure by feeding practices in babies aged 0-6 months.

This study was conducted to estimate the daily dietary intakes of melamine for human milk-fed (HMF) babies and mixed-fed (MF) babies. It was carried out in 70 mother-baby pairs (40 babies in the HMF group and 30 babies in the MF group). Human milk, formula milk, and baby urine samples were collected to assess the dietary exposure of babies. Melamine concentrations were analyzed by using a competitive enzyme-linked immunosorbent assay. Melamine was determined in 82.5 % of the human milk samples in the HMF group (median: 0.75 µg/L) while it was present in 96.7 % of human milk samples (median: 1.25 µg/L) and 96.7 % in formula milk samples (median: 0.95 µg/kg) in the MF group. The mean urinary melamine concentration of HMF babies (1.20 ± 0.21 µg/L) was not significantly different than MF babies (1.35 ± 0.49 µg/L). Melamine exposure was calculated as 0.12 µg/kg bw/day and 0.24 µg/kg bw/day in HMF and MF babies, respectively. Melamine exposure in both groups was below the tolerable daily intake. There were no significant associations between melamine exposure and various features of babies and mothers. As a result, it can be suggested that Turkish babies (aged 0-6 months) are not at risk for high melamine exposure through the diet.

Protective effect of cinnamic acid on orthophenylphenol-induced oxidative stress in rats.

This study aimed to evaluate the protective effect of cinnamic acid (CA) on orthophenyl-phenol (OPP)-induced oxidative stress in rats. Thirty-two Sprague-Dawley male rats were divided into four groups as control, OPP, CA and OPP + CA groups. The animals in control, OPP and CA groups were received corn oil, OPP (700 mg kg-1 dissolved in corn oil) and CA (200 mg kg-1) by gavage for 21 days, respectively. The animals in OPP + CA group were received CA for 3 days and from day 4; OPP and CA were applied together daily until day 25. Blood and liver samples were collected at the end of experiment for measurement of aminotransferases, creatinine (CREA), catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), reduced glutathione (GSH) and malondialdehyde (MDA). The OPP-induced high serum activities of aminotransferases and level of CREA were reduced significantly by CA administration. The OPP induced significant increases of CAT activities and MDA levels in serum and liver tissue samples. Moreover, OPP significantly decreased GSH levels as well as GSH-Px and SOD activities. Pre-treatment with CA ameliorated the GSH levels along with GSH-Px and SOD activities compared to OPP-receiving rats. On the other hand, CAT activities and MDA levels significantly decreased following the pre-treatment with CA compared to OPP-receiving rats. It has been determined that OPP causes oxidative stress and lipid peroxidation in blood and liver tissues and creates changes in anti-oxidant defense enzymes. Pre-treatment with CA reduces lipid peroxidation and provides protective effect against oxidative stress.

Neurological Effects of SARS-CoV-2 and Neurotoxicity of Antiviral Drugs Against COVID-19.

Severe Acute Respiratory Syndrome (SARS) is caused by different SARS viruses. In 2020, novel coronavirus (SARS-CoV-2) led to an ongoing pandemic, known as "Coronavirus Disease 2019 (COVID-19)". The disease can spread among individuals through direct (via saliva, respiratory secretions, or secretion droplets) or indirect (through contaminated objects or surfaces) contact. The pandemic has spread rapidly from Asia to Europe and later to America. It continues to affect all parts of the world at an increasing rate. There have been over 92 million confirmed cases of COVID-19 by mid-January 2021. The similarity of homological sequences between SARS-CoV-2 and other SARSCoVs is high. In addition, clinical symptoms of SARS-CoV-2 and other SARS viruses show similarities. However, some COVID-19 cases show neurologic signs like headache, loss of smell, hiccups and encephalopathy. The drugs used in the palliative treatment of the disease also have some neurotoxic effects. Currently, there are approved vaccines for COVID-19. However, there is a need for specific therapeutics against COVID-19. This review will describe the neurological effects of SARS-CoV-2 and the neurotoxicity of COVID-19 drugs used in clinics. Drugs used in the treatment of COVID-19 will be evaluated by their mechanism of action and their toxicological effects.

Adverse Effects of COVID-19 Treatments: A Special Focus on Susceptible Populations.

On December 2019, the world faced a new pandemic caused by a novel type of coronavirus, namely severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). This disease is named as "coronavirus disease 2019 (COVID-19)." This RNA virus infected millions of people around the world causing millions of deaths. It takes approximately 8-10 years to develop a new drug and it seems hard to have a specific pharmaceutical agent against COVID-19. So far, there is only one drug that has applied for registration. The drugs used in clinics against COVID-19 were approved for malaria, human immunodeficiency syndrome (HIV), influenza A and B, and other viral diseases. All these drugs for COVID-19 treatment are being applied according to "drug repurposing (drug repositioning)" strategy. However, they could cause some severe adverse effects on susceptible populations. In some cases, patients can survive after disease. However, the adverse effects of these drugs may lead to morbidity and mortality later. In this review, drugs used against COVID-19 in clinics, their mechanisms of action and possible adverse effects on susceptible populations will be discussed.