Polymerizable sol-gel synthesis of dark-visible light antibacterial magnetically-recoverable AgBr-loaded iron oxide/alumina nanocomposite.

The demand for a facile approach for synthesizing multifunctional nanocomposites is increasingly vital across diverse applications. In this study, a polymerizable sol-gel synthesis has been reported to obtain nanocomposites of magnetic iron oxide deposited over alumina nanopowder. The synthesis is mediated by the deposition of a calculated amount of iron(III) methacrylate, along with ethylene glycol dimethacrylate crosslinker, over alumina nanopowder, followed by thermally-inducing free radical polymerization at 125 °C for 30 min. The powder thus obtained has been subjected to calcination at 400 °C for 150 min and the resultant nanocomposites were characterized using wide-angle x-ray scattering, attenuated total reflectance-Fourier transform infrared spectroscopy, x-ray photoelectron spectroscopy, field-emission scanning electron microscopy, ultraviolet-diffuse reflectance spectroscopy, vibrating sample magnetometer and Brunauer-Emmett-Teller surface area measurements. The nanocomposites containing 15 and 20 wt% of iron oxide have been found to exhibit a saturation magnetization (Ms) value ranging from 12 to 14 emu g-1. To the nanocomposite containing 20 wt% of iron oxide, 5 wt% of AgBr was loaded through thoroughly mixing a surfactant-based precursor, silver-tetraoctyl ammonium bromide (Ag-TOAB), followed by thermolysis. All the nanocomposites have been studied for their antibacterial activity against a representative gram-negative bacterium,Escherichia coli, under dark and visible light conditions. While a 3 mg ml-1loading of the AgBr-loaded nanocomposite has exhibited complete clearance of the bacterial growth by 90 min in the dark, a similar activity has been observed in 60 min under light. The study has revealed the multifunctionality and high potential of the AgBr-loaded iron oxide/alumina nanocomposite as a promising dual-mode antibacterial and magnetically recoverable photocatalyst material.

Targeting mitochondria with folic acid and vitamin B12 ameliorates nicotine mediated islet cell dysfunction.

Nicotine, one of the well-known highly toxic components of cigarette smoke, causes a number of adverse health effects and diseases. Our previous study has shown that nicotine induces reactive oxygen species (ROS) in islet cell and disrupts islet cell mitochondrial membrane potential (ΔΨm). However, supplementation with folic acid and vitamin B12 were found effective against nicotine induced changes in pancreatic islet cells. But the toxicological effects and underlying mechanisms of nicotine-induced mitochondrial dysfunction is still unknown. In this study, nicotine exposure decreases mitochondrial enzymes (pyruvate dehydrogenase, alpha-ketoglutarate dehydrogenase, aconitase, malate dehydrogenase) activities by increasing cytosolic Ca2+ level which may contribute to increased mitochondrial ROS production by raising its flow to mitochondria. This in turn produces malondialdehyde and nitric oxide (NO) with a concomitant decrease in the activities of antioxidative enzymes and glutathione levels leading to loss of ΔΨm. Simultaneously, nicotine induces pancreatic islet cell apoptosis by modulating ΔΨm via increased cytosolic Ca2+ level, altered Bcl-2, Bax, cytochrome c, caspase-9, PARP expressions which were prevented by the supplementation of folic acid and vitamin B12 . In conclusion, nicotine alters islet cell mitochondrial redox status, apoptotic machinery, and enzymes to cause disruption in the ΔΨm and supplementation of folic acid and vitamin B12 possibly blunted all these mitochondrial alterations. Therefore, this study may help to determine the pathophysiology of nicotine-mediated islet cell mitochondrial dysfunction.

Association between duration of coal dust exposure and respiratory impairment in coal miners of West Bengal, India.

Purpose. The prevalence and severity of respiratory disorders are very high among coal miners as continuous exposure of workers in such an environment leads to accumulation of dust in the lungs. This study was designed to assess the prevalence of lung function impairment and to determine whether there is any correlation between dust exposure duration and lung function indices. Materials. Two hundred and thirty underground coal dust-exposed workers and 130 age-matched non-exposed workers were recruited from an underground mine in West Bengal, India. A spirometry test was performed for lung function and also basic information on personnel's dust exposure, smoking and respiratory morbidity was collected. Student's t test, Pearson's correlation coefficient (r), uncorrected Pearson's χ2 test and Fischer's exact test were performed for statistical analysis. Results. Lung function indices were significantly (p < 0.050) impaired between the exposed (43.91%) and non-exposed (23.85%) groups. In addition, highly significant decrements in the pulmonary volumes of exposed subjects were also noted. Furthermore, a high negative correlation was observed between spirometric results and exposure time in the exposed group compared with the non-exposed group. Conclusion. This study suggested a positive relationship between exposure time and lung function deterioration.

Combined effect of coal dust exposure and smoking on the prevalence of respiratory impairment among coal miners of West Bengal, India.

Accelerating prevalence of coal workers pneumoconiosis is considered as a serious occupational health problem. This cross-sectional study was designed to determine the prevalence of lung function impairment of underground coal miners in West Bengal, India. A total of 230 underground coal dust-exposed subjects and 130 nonexposed subjects were examined for lung function test and also information on sociodemographic characteristics, addiction, respiratory morbidity, personnel protective equipment and dust exposure were collected. Lung function impairment was significantly higher in exposed group than nonexposed group and personnel dust exposure level were exceeded above the NIOSH recommended level. In addition, respiratory ailments were found to be higher in exposed group than the nonexposed group. So, this study has established the need for an advanced understanding of the quantifiable and measurable remedies for protection of lung disorder of coal mine workers.

Radioprotective effect of ethanolic extract of Alocasia indica on γ-irradiation-induced reproductive alterations in ovary and uterus.

Evaluation of the modulatory effect of ethanolic extract of Alocasia indica tuber (EEAIT) against γ-irradiation induced ovarian and uterine toxicity. Extract preparation was done by 80% hydro-ethanol using Soxhlet apparatus. EEAIT was administered to female Swiss albino mice (n = 5) daily (200 and 400 mg/kg body weight/d) for 7 days before γ-irradiation exposure (2.9 Gy). FSH, LH, estrogen, progesterone, cytokine levels, and oxidative stress parameters were measured after 24 hours of γ-irradiation. Histology, folliculogenesis, viability of granulosa cells, ROS measurement by flow cytometry, western blot of P450scc, P45017A1, 3ß HSD and SF 1 were also performed. In addition, fertility status was assessed by fecundability and fecundity. The results showed that EEAIT exhibit a strong radioprotective activity by reducing the oxidative stress and thereby restored the ovarian and uterine alterations. EEAIT also improved the abnormality in follicle development, restored altered gonadal hormones and cytokines levels, increase the fertility status, reducing ROS level of granulosa cells with increasing granulosa cells viability and steroidogenic enzyme activity as compared to control. So EEAIT showed a radioprotective effect on γ-irradiation induced ovarian and uterine damage. Our results suggested that Alocasia indica tuber can be a potential radioprotector to prevent female infertility.

Possible involvement of iNOS and TNF-α in nutritional intervention against nicotine-induced pancreatic islet cell damage.

Nicotine is the more abundant and most significant components of cigarette smoke. Epidemiological evidence strongly suggests an association between cigarette smoking and pancreatic injury. Although effects of smoking on endocrine pancreas are still controversial Here, we examined the impact and underlying mechanisms of action of folic acid and vitamin B12 on nicotine induced damage in pancreatic islets of rats. Male Wistar rats were treated with nicotine (3mg/kg body weight/day, intraperitonealy) with or without folic acid (36µg/kg body weight/day, orally) and vitamin B12 (0.63µg/kg body weight/day, orally) for 21days. Supplementation with folic acid and vitamin B12 suppressed the nicotine induced changes in HbA1c, insulin, TNF-α, IL-6, generation of reactive oxygen species, and attenuated the changes in markers of oxidative stress. Moreover, folic acid and vitamin B12 also counteracted the increased expression of protein and mRNA contents of TNF-α and iNOS produced by nicotine. Further, folic acid and vitamin B12 in combination limits the nicotine induced changes in cell cycle and excessive apoptosis of the pancreatic ß-cells and also successfully blunted the nicotine induced alteration in loss of mitochondrial membrane potential. In conclusion, data demonstrate that folic acid and vitamin B12 may be possible nutritional intervention against cellular oxidative stress, which is a critical step in nicotine-mediated islet injury, and improves islet cell functional status by scavenging free radicals and by inhibiting the generation of pro-inflammatory mediators.