The role of N-acetylcysteine (NAC), a glutathione (GSH) precursor, was investigated in protection against isoniazid-(INH) and rifampicin-(RIF) induced oxidative hepatic injury in young Wistar rats. The hepatotoxic dose of INH and RIF was 50 mg kg-1 day-1 each and the hepatoprotective dose of NAC was 100 mg kgday-. All drugs were administered intraperitoneally (i.p.) in sterile water (4.0 ml kg-1 day-1) over a period of 3 weeks. Status of oxidative/antioxidative profiles was the mechanistic approach to assess the hepatotoxicity and/or hepatoprotection. The oxidative injury in INH-RIF co-exposed animals was closely associated with significant decline of GSH and related thiols, as well as with compromised antioxidant enzyme system. The oxidative stress was further supported by increased lipid peroxidation observed in these animals. The co-administration of NAC prevented the induction of oxidative stress in INH-RIF co-exposed animals. The amelioration of oxidative stress by NAC was faithfully reflected as normal morphology in these animals, except the presence of mild degree of portal triaditis in one animal co-exposed to INH-RIF and NAC. In contrast, the animals co-exposed to INH-RIF alone showed histological lesions which ranged from intralobular inflammation to patchy necrosis. These results suggest that INH-RIF-induced oxidative injury can be prevented by supporting the cellular antioxidant defense mechanism by NAC.

A high prevalence of VDD in critically ill children with sepsis was found but it was not associated with greater severity of illness or other clinical outcomes.

Globally, both obesity and underweight are severe health risks for various diseases. The current study systematically examined the emerging evidence to identify an association between body mass index (BMI) and COVID-19 disease outcome. Online literature databases (e.g., Google Scholar, PubMed, MEDLINE, EMBASE, Scopus, Medrixv and BioRixv) were screened following standard search strategy having the appropriate keyword such as “Obesity”, “Underweight”, “BMI”, “Body Mass Index”, “2019-nCov”, “COVID-19, “novel coronavirus”, “coronavirus disease”. Studies published till 20 th April 2020 were included without language restriction. These studies include case reports, case series, cohort, and any other which reported BMI, overweight/obesity or underweight, and its complication with COVID-19 disease. This study observed COVID-19 infection among BMI < 25 kg/m 2 with prevalence of 0.60 (95%CI: 0.34–0.86, I 2 = − 76.77) as compared to the 0.34 (95%CI: 0.23–0.44, I 2 = 53.45% heterogeneity) having BMI > 25 kg/m 2 . The results of the current study show that BMI plays a significant role in COVID-19 severity in all age groups, especially the older individuals. A panel of doctors and nursing staff should review COVID-19 patients with higher BMI with other co-morbidities (diabetes and hypertension), and they should be given increased vigilance, priority in testing, and treatment to control the associated co-morbidities. Further, the COVID-19 patients whose illness entered 7–10 days, age > 50 years, and elevated CRP levels should be given additional medical considerations. Our finding showed that the population and patients with high BMI have moderate to high risk of medical complications with COVID-19, and hence, their health status should be monitored more frequently including monitoring of blood pressure and blood glucose.

Animal models of copper toxicosis rarely exhibit neurological impairments and increased brain copper accumulation impeding the development of novel therapeutic approaches to treat neurodegenerative diseases having high brain Cu content. The aim of this study was to investigate the effects of intraperitoneally injected copper lactate (0.15 mg Cu/100 g body weight) daily for 90 days on copper and zinc levels in the liver and hippocampus, on biochemical parameters, and on neurobehavioral functions (by Morris water maze) of male Wistar rats. Copper-administered animals exhibited significantly decreased serum acetylcholinesterase (AChE) activity and impaired neuromuscular coordination and spatial memory compared to control rats. Copper-intoxicated rats showed significant increase in liver and hippocampus copper content (99.1 and 73 % increase, respectively), 40.7 % reduction in hepatic zinc content, and interestingly, 77.1 % increase in hippocampus zinc content with concomitant increase in copper and zinc levels in serum and urine compared to control rats. Massive grade 4 copper depositions and grade 1 copper-associated protein in hepatocytes of copper-intoxicated rats were substantiated by rhodanine and orcein stains, respectively. Copper-intoxicated rats demonstrated swelling and increase in the number of astrocytes and copper deposition in the choroid plexus, with degenerated neurons showing pyknotic nuclei and dense eosinophilic cytoplasm. In conclusion, the present study shows the first evidence in vivo that chronic copper toxicity causes impaired spatial memory and neuromuscular coordination, swelling of astrocytes, decreased serum AChE activity, copper deposition in the choroid plexus, neuronal degeneration, and augmented levels of copper and zinc in the hippocampus of male Wistar rats.

The present study reports the simultaneous analysis of 26 physiological amino acids in plasma along with total cysteine and homocysteine by high-performance liquid chromatography (HPLC) employing 6-aminoquinolyl-N-hydroxysuccinimidyl carbamate (AQC) as precolumn derivatizing reagent. Separations were carried out using Lichrospher 100 RP-18e (5 μm) 250 × 4.0 mm column connected to 100 CN 4.0 × 4.0 mm guard column on a quaternary HPLC system and run time was 53 min. Linearity of the peak areas for different concentrations ranging from 2.5 to 100 pmol/μL of individual amino acids was determined. A good linearity (R (2) > 0.998) was achieved in the standard mixture for each amino acid. Recovery of amino acids incorporated at the time of derivatization ranged from 95 to 106 %. Using this method we have established the normative data of amino acids in plasma, the profile being comparable to the range reported in literature and identified cases of classical homocystinuria, cobalamin defect/deficiency, non-ketotic hyperglycinemia, hyperprolinemia, ketotic hyperglycinemia, urea cycle defect and maple syrup urine disease.