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In December 2019, a new type of SARS corona virus emerged from China and caused a globally pandemic corona virus disease (COVID-19). This highly infectious virus has been named as SARS-CoV-2 by the International Committee of the Taxonomy of Viruses. It has severely affected a large population and economy worldwide. Globally various scientific communities have been involved in studying this newly emerged virus and is lifecycle. Multiple diverse studies are in progress to design novel therapeutic agents, in which understanding of interactions between the target and drug ligand is a significant key for this challenge. Structures of proteins involved in the life cycle of the virus have been revealed in RCSB PDB by researchers. In this study, we employed molecular docking study of 4-Acetamido-3-nitrobenzoic acid (ANBA) with corona virus proteins (spike protein, spike binding domain with ACE2 receptor and Main protease, RNA-dependent RNA polymerase). Single crystal X-ray analysis and density functional theory calculations were carried out for ANBA to explore the structural and chemical-reactive parameters. Intermolecular interactions which are involved in the ligand-protein binding process are validated by Hirshfeld surface analysis. To study the behaviour of ANBA in a living organism and to calculate the physicochemical parameters, ADMET analysis was done using SwissADME and Osiris data warrior tools. Further, Toxicity of ANBA was predicted using pkCSM online software. Based on the molecular docking analysis, we introduce here a potent drug molecule that binds to the COVID-19 proteins.Communicated by Ramaswamy H. Sarma.

A new organoclay, consisting of montmorillonite modified by a hexadecyl trimethyl ammonium (HDTMA) microemulsion, was synthesized, characterized and used as an adsorbent for the removal of o-nitrobenzoic acid from aqueous solution. Adsorption kinetics, isotherms and effects of operating variables, such as adsorbent dosage, ionic strength and initial solution pH, were also investigated. The results of Fourier transform infrared spectroscopy (FTIR), X-ray diffraction (XRD) analysis and BET surface area determination indicated that HDTMA molecules had entered into the interlayer of the montmorillonite. The optimized experimental conditions for the adsorption of o-nitrobenzoic acid by montmorillonite modified by HDTMA microemulsion were 0.5 g adsorbent dosage, 0.4 mL of 0.1 mol lbL(-1) CaCl2 solution, initial solution pH of 6.0 and contact time of 6 h. The adsorption isotherms of o-nitrobenzoic acid fitted the Langmuir model well (R2 = 0.9880). The adsorption kinetics data fitted the pseudo-second-order equation (R2 = 0.9999). These above results indicate that montmorillonite modified by an HDTMA microemulsion can be used as adsorbent for o-nitrobenzoic acid because of its high adsorption capacity and low cost.

The purpose of the present study is to observe the role of volume-sensitive Cl(-) channels in carboplatin-induced apoptosis in the human lung adenocarcinoma cell line A549 cells. Using patch clamp and apoptosis assays, we found that A549 cells underwent the process of apoptotic volume decrease (AVD) and apoptosis when treated with carboplatin or staurosporine (STS). This AVD and apoptosis process were blocked by chloride channel blockers, 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS) and 5-nitro-2-(3-phenyl propylamino)-benzoate (NPP B). Both carboplatin and STS treatment activated a Cl(-) current, which shows similar properties to hypotonicity-induced volume-sensitive Cl(-) current in A549 cells. In addition, carboplatin pretreatment augmented the magnitude of the hypoosmotic-induced volume-sensitive Cl(-) current. These results suggest that volume-sensitive Cl(-) channels may be responsible for the carboplatin-induced apoptosis in A549 cells by inducing the AVD process.

We present the clinical data of five infants with type I (hepato-renal) tyrosinaemia on NTBC therapy. All presented initially at the local hospital in the 1st year of life with progressive abdominal distension owing to hepato-splenomegaly and with radiological evidence of liver cirrhosis, except for one child who was diagnosed during screening because of an affected sibling. Age at commencement of NTBC therapy ranged from 6 to 30 months. All infants showed remarkable improvement within 2-6 months of starting NTBC treatment, except one who died 2 months after commencement of therapy from uncontrolled liver failure, severe coagulopathy and Streptococcus pneumoniae septicaemia. NTBC treatment along with a phenylalanine- and tyrosine-restricted diet has effectively reversed most clinical manifestations of this disease. To date, none of our patients has developed hepatic carcinoma and NTBC was well tolerated without side-effects. NTBC is costly but life-saving and is an obvious alternative to more hazardous liver transplantation.

Hereditary tyrosinaemia type I is the most common of the diseases caused by defects in tyrosine metabolism. The underlying genetic defect is a mutation in the gene for fumarylacetate hydrolase (FAH), and more than 30 different mutations in this gene have been identified. The main clinical consequences of this defect include hepatic involvement, with a high risk for liver cancer, and renal tubular dysfunction. Restriction of phenylalanine and tyrosine from the diet along with supportive measures can ameliorate the symptoms, but cure has so far been possible only with liver transplantation. Recent discovery of a pharmacological treatment with a peroral inhibitor of tyrosine catabolic pathway, 2-(2-nitro-4-trifluoromethylbenzoyl)-1,3-cyclohexanedione (NTBC), offers a new promising tool for the treatment of patients with hereditary tyrosinaemia type I. Mouse models of FAH deficiency have been successfully used in experimental gene therapy, and these studies indicate that future management of tyrosinaemia with a gene therapeutic approach may become feasible.

On studying the thermal behaviour of a series of 1,1,2,2-tetrahydro-perfluoroalkyl 4-nitrobenzoates it was found that the decyl and dodecyl compounds showed smectic mesophases. This illustrates that a polar substituent in the 3-position of the aromatic ring for 1,1,2,2-tetrahydroperfluoroalkylbenzoates is not a requirement for thermotropic behaviour.

Laboratory experiments were conducted to study the degradation of acifluorfen 5‐[2‐chloro‐4‐ (trifluoromethyl)‐phenoxy]‐2‐nitrobenzoic acid by a mixed microbial population. Concentrations of acifluorfen up to 100 mg/1 had no inhibitory effect on the growth of microbial culture. The microorganisms degraded acifluorfen through a cometabolic process in presence of 2‐nitrobenzoate. The degradation rate of acifluorfen, determined by liquid chromatography analysis in batch cultures incubated under oxygen and oxygen‐limited conditions were compared. The degradation was slower under oxygen than oxygen‐limited conditions. Aminoacifluorfen was produced in both conditions.

Methyl and ethyl-4-[(4′-substituted phenylsulfonyl)methyl]-3-nitrobenzoates and the corresponding sulfinyl derivatives have been synthesized. The structure of these esters were proved by IR, NMR and mass spectra. A linear relationship between δ-ppm values of the benzylic protons and [sgrave]-Hammett values of the 4′-substituents has been found. The carbon-sulfur bond fission with 5% sodium hydroxide solution in addition to the alkaline ester hydrolysis is discussed.

The thermal properties of 4-octyloxyphenyl 4-(4-R-3-nitrobenzoyloxy) benzo-ates (1) and 4-(4-octyloxybenzoyloxy)phenyl 4-R-3-nitrobenzoates (2) have been examined, where R = hydrogen, halogens, alkyl and alkoxy groups. The derivatives of compound 1 incorporating hydrogen, halogens, methoxy and nitro groups show a smectic A phase having a bilayer arrangement, and the others with a long alkoxy group show the SA phase with the monolayer arrangement. The derivatives of compound 2 incorporating halogens, and the nitro group show the SA phase with the monolayer arrangement. The alkoxy derivatives show a smectic C phase as well as the nematic phase. The nitro group at the lateral position tends to increase the ratio of the SA-N transition temperature to the N-I. The effect of the nitro group on the smectic properties has been discussed in terms of the structural and electrostatic nature of the nitro group.

Pulse radiolysis was used to establish one-electron transfer equilibria between radical cations of methyl or benzyl viologens (V2+) and nitroaryl compounds (ArNO2): a nitroimidazole (misonidazole or metronidazole), 4-nitrobenzoate or nitrofurazone. The equilibrium constants in water at pH 8 were estimated over the temperature range approximately 5 to 75 degrees C. The difference delta E in mid-point one-electron reduction potentials between the nitro compounds and the viologens varied with temperature T; increasing temperature made the nitro compounds apparently less electron-affinic compared to the effects of temperature on the viologen potential. Values of delta(delta E)/delta T were in the range -0.7 to -1.1 mV K-1 at 25 degrees C. If delta[E(V2+/V.+)]/delta T = -0.9 mV K-1 for methyl viologen then delta[E(ArNO2/ArNO2.-)]/delta T is about -2 mV K-1 for these compounds.

1. 4-Nitrobenzoic acid was excreted in rat urine as 4-aminobenzoic acid and its conjugates after oral (20% dose) and intraperitoneal (17% dose) administration. Suppression of gut microflora by oral administration of antibiotics decreased the reduction in vivo (5% dose was reduced after high dose antibiotics and 13% after low dose antibiotics). The liver, intestinal wall and content of the caecum and colon reduced 4-nitrobenzoic acid extensively in vitro. Pre-treatment with antibiotics decreased the activities of intestinal wall and hind gut contents but not of liver.2. 3-Nitrobenzoic acid was excreted in rat urine as 3-aminobenzoic acid and its conjugates after oral administration to normal (16% dose) and low dose antibiotic-treated animals (7% dose). 2-Nitrobenzoic acid underwent less reduction in vivo in normal animals (10% dose) and this was largely suppressed by low dose antibiotic treatment (1% of dose). The abilities of liver, intestinal wall and caecum and colon contents to reduce 3-nitrobenzoic ac...

1. The substrate specificity of nitro-reductase from Ascaris lumbricoides varsum was determined. This enzyme reduced nitrobenzene, 4-nitrohippuric acid and the isomers of nitrophenol, nitroanisole, nitrobenzoic acid, nitrobenzaldehyde and nitrobenzyl alcohol. The same enzyme preparation reduced azobenzene, 4-dimethylaminoazobenzene and 1,2-dimethyl-4-(4-carboxyphenylazo)-5-hydroxybenzene. Nitrobenzaldehyde isomers were not reduced to the alcohols. 2. The products of nitro- and azo-reduction were the corresponding amines, no hydroxylamino or hydrazo compounds were detected. 3. The pH optima and cofactor requirements were the same for both azo- and nitro-reduction and neither reaction was inhibited by oxygen. 4. Ammonium sulphate fractionation failed to separate azo- and nitro-reductase activities. The molecular weight of both azo- and nitro-reductase was about 130 000.

1. Reductive metabolism of p-nitrobenzoic acid and neoprontosil in rat liver microsomes was studied in the presence of haemin, haemoglobin and myoglobin. 2. Microsomal nitro reduction is enhanced 4-fold in the presence of haemoglobin, whereas azo reduction is not affected. 3. Microsomal nitro reduction is enhanced to a similar extent by haemoglobin, haemin and boiled haemoglobin, whereas myoglobin is about half as active. 4. Maximal enhancement of microsomal nitro reductase activity by haemoglobin is achieved at high substrate concentration (6 mM) and low microsomal protein concentration (0.5--1.0 mg/ml). 5. Control microsomal nitro reduction as well as the haemoglobin-enhanced microsomal nitro reduction are inhibited completely by O2 and CO whereas potassium azide as a ligand of ferric haem iron is a less potent inhibitor.

1. Hepatic azo and nitro reductase activities were studied in the perfused rat liver under normal and restricted oxygen supply. 2. Formation of sulphanilamide or p-aminobenzoic acid from neoprontosil or p-nitrobenzoic acid under aerobic conditions of liver perfusion was negligible, even at a reduced oxygen saturation of a pO2 of 300 mm Hg in the haemoglobinfree perfusion system. At a pO2 of 200 mm Hg reductase activities were almost maximal. 3. Conjugation of sulphanilamide (0-08 mM) was similar under aerobic and anaerobic conditions. Hepatic elimination of p-aminobenzoic acid (0-08 mM) showed an oxygen-dependent increase for 15 min after addition of substrate. 4. p-Nitroanisole demethylation was inhibited 80% under hypoxic perfusion at 200 mm Hg pO2 and was completely inhibited after gassing with anoxic mixtures. 5. Restitution of aerobic conditions after 30 min anaerobic perfusion restored hepatic respiration, lactate pyruvate ratio, and pH value to levels found under aerobic conditions, but bile flow remained 50% reduced.

Twelve 4-alkoxyphenyl esters of 4-nitrobenzoic acid have been synthesized. The mesophases have been identified and the transition temperatures and enthalpies determined. The above series shows considerable similarity to the reverse analogues, i.e., the 4-nitrophenyl 4- n-alkoxybenzoates.