Sainath Babu

Prooxidant actions of bisphenol A (BPA) phenoxyl radicals: implications to BPA-related oxidative stress and toxicity

Abstract We investigated the prooxidant effects of bisphenol A (BPA) phenoxyl radicals in comparison with the phenoxyl radicals of 3-tert-butyl-4-hydroxyanisole (BHA), 2,6-di-tert-butyl-methylphenol (BHT) and 4-tert-butylphenol (TBP). The phenoxyl radicals, generated in situ by 1-electron oxidation of the corresponding phenol, were allowed to react with reduced nicotinamide adenine dinucleotide phosphate (NADPH) and rifampicin. The antioxidant activity of various phenols was examined based on the reduction of 2,2′-diphenyl-1-picrylhydrazyl radical (DPPH). It was found that the prooxidant activity of BPA phenoxyl radicals far exceeded those of BHA and BHT of phenoxyl radicals. Unlike Trolox, BPA showed minimal DPPH scavenging activity. The strong prooxidant properties of BPA phenoxyl radicals propelled us to study the markers of cellular oxidative stress in GT1-7 hypothalamic neurons exposed to BPA. It was observed that neuronal cells exposed to BPA had increased generation of intracellular peroxides and mitochondrial superoxide (). The formation of peroxides and were time- and dose-dependent and that co-incubation with N-acetyl-l-cysteine or Trolox greatly lowered their levels. The results of the present study are consistent with emerging evidence that human populations (non-institutionalized) having higher levels of urinary BPA also have increased levels of oxidative stress markers and are prone to higher risk of cardiovascular diseases, diabetes and abnormalities in hepatic enzymes.

Unusually high levels of bisphenol A (BPA) in thermal paper cash register receipts (CRs): development and application of a robust LC-UV method to quantify BPA in CRs

Abstract We have developed a simple, reversed-phase high-performance liquid chromatography (RP-HPLC) method for the determination of bisphenol A (BPA) in thermal paper cash register receipts (CRs). The method is suitable for analysis of other types of bisphenols and it involves an overnight extraction of CRs with acetonitrile (AN) at 50 °C followed by the HPLC analysis on a Supelcosil LC18 column (150 × 4.6 mm, particle size: 5 μ) using 50% AN in water as the mobile phase (5 min, isocratic). The composition of AN in the mobile phase changed to 100% over a 10 min period (linear gradient) and then held at 100% AN for 10 min (isocratic). The flow rate was set at 1 mL/min (injection volume: 20 μL) and the eluent was monitored at 234 nm. The authentic BPA eluted with a retention time of 5.9 min and gave a linear detector response in the concentration range of 0.23–50 mg/L. BPA in the CR extracts also eluted with the same retention and had identical absorbance properties as the standard. When CR extracts were co-injected with authentic BPA, they were resolved as a single peak. Further, GC/MS/EI analysis of authentic BPA and the HPLC-purified CR extracts have identical ion chromatograms and fragmentation of the molecular ion (m/z = 228). We have analyzed 170 CRs collected from 62 different vendors including supermarkets, fast food restaurants, gas stations and banking outlets. Almost all cash receipts (n = 168) showed the presence of BPA in the concentration range of 0.45–4.26% (M ± SD, 1.54 ± 0.73%).

Intracellular oxidative stress and cytotoxicity in rat primary cortical neurons exposed to cholesterol secoaldehyde

Cholesterol secoaldehyde (ChSeco or 3beta-hydroxy-5-oxo-5,6-secocholestan-6-al) has been shown to induce Abeta aggregation and apoptosis in GT1-7 hypothalamic neurons. The present study was undertaken to evaluate the effects of ChSeco on rat primary cortical neuronal cells. ChSeco was cytotoxic at concentrations ranging from 5 to 20 microM, while cholesterol of comparable concentrations showed little or no toxicity. In ChSeco-exposed neuronal cells, there was an increased formation of intracellular peroxide or peroxide-like substance(s), the levels of which were comparable to those found in typical menadione exposures. There was a loss in the mitochondrial transmembrane potential, the extent of which was dependent on concentration of ChSeco employed. Pre-treatment with N-acetyl-L-cysteine (5 mM; 1 h) offered protection against the cytotoxicity and the generation of intracellular oxidants. Cytotoxicity of ChSeco was evidenced by the loss of axonal branches and also condensed apoptotic nuclei in these cells. Immunohistochemical analysis revealed a decreased intracellular Abeta42 staining proportional to the loss in the axonal out growth and dendritic branches. The observed decrease in Abeta42 has been suggested to be due to loss of integrity of dendrites and the plasma membrane, possibly resulting from increased production of reactive oxygen species.

3,3′-Dinitro­bis­phenol A

The title compound [systematic name: 2,2′-dinitro-4,4′-(propane-2,2-diyl)diphenol], C15H14N2O6, crystallizes with two molecules in the asymmetric unit. Both have a trans conformation for their OH groups, and in each, the two aromatic rings are nearly orthogonal, with dihedral angles of 88.30 (3) and 89.62 (2)°. The nitro groups are nearly in the planes of their attached benzene rings, with C—C—N—O torsion angles in the range 1.21 (17)–4.06 (17)°, and they each accept an intramolecular O—H⋯O hydrogen bond from their adjacent OH groups. One of the OH groups also forms a weak intermolecular O—H⋯O hydrogen bond.

4-Hydr­oxy-3-meth­oxy-5-nitro­aceto­phenone (5-nitro­apocynin)

The title molecule, C9H9NO5, is close to planar (r.m.s. deviation from the mean plane of the non-H atoms = 0.058 Å). The OH group forms a bifurcated O—H⋯(O,O) hydrogen bond, with the intramolecular component to a nitro O atom and the intermolecular component to a keto O atom, the latter resulting in chains along [20]. A C—H⋯O interaction reinforces the packing.