Exposure of active pharmaceutical compounds (APCs) to the environment during human use is of potential importance in the emergence of drug resistance, changing soil microbiota and their residual effect on living organisms. Thus, this study aimed to assess the extent of exposure of APCs in the hydrologic cycle in and around New Delhi. This study analyzed the presence of 28 drugs from different classes in the surface water (river Yamuna) and aquifers collected from 48 places in Delhi (within the radius of 40 km). The collected water samples were quantified for APCs content using LC-MS/MS. This study revealed that aquifers are extensively affected in most areas based on the accumulation of APCs in water resources to the levels > 0.01 μg/L. Interestingly, a geographical plot of total APCs studied indicated clustering in aquifers with such high levels closer to an unscientific landfill. This 30-year-old un-segregated landfill is found to drain leachate into surface water that had high APCs. This study further revealed that apart from therapeutic usage, the main source of ecological exposure could be due to the disposal of unused and expired pharmaceutical compounds into landfills. For the first time, this study revealed the existence of antimicrobial agents and other APCs in the aquifers of Delhi with levels > 0.1 μg/L, which is a matter of serious concern in terms of multi-drug resistance and other environmental perils. This study warrants the enforcement of regulations for the disposal of unused/expired APCs in high-density population areas.

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Inflammation, a common denominator among the diverse list of neurodegenerative diseases, has recently been implicated as a critical mechanism responsible for the progressive nature of neurodegeneration. Microglias are the resident innate immune cells in the central nervous system and produce a barrage of factors (ILs, TNF α, NO, PGs, SOD) that are toxic to neurons. Evidence supports that the unregulated activation of microglia, in response to environmental toxins, endogenous proteins and neuronal death, results in the production of toxic factors that propagate neuronal injury. Herbal medicine has long been used to treat neural symptoms. Although the precise mechanisms of action of herbal drugs have yet to be determined, some of them have been shown to exert anti-inflammatory and / or antioxidant effects in a variety of peripheral systems. Now, as increasing evidence indicates that neuroglia-derived chronic inflammatory responses play a pathological role in the central nervous system, anti-inflammatory herbal medicine and its constituents are being proved to be potent neuroprotectors against various brain pathologies. Structural diversity of medicinal herbs makes them a valuable source of novel lead compounds against therapeutic targets that are newly discovered by genomics, proteomics and high-throughput screening. In the following review, we discuss the common thread of microglial activation across numerous neurodegenerative diseases, define current perceptions of how microglia are damaging neurons and explain how the microglial response to neuronal damage results in a self-propelling cycle of neuron death. This article synthesizes what we know about these destructive processes, while offering an insight into a new avenue of treatment involving phytochemicals and other nutrients.

The aim of this study was to investigate the potent neuroprotective property of ethanol extract of Ocimum sanctum (EEOS) leaf (Holy basil, Family: Labiataea) against excitotoxicity induced neurodegeneration by using monosodium-L-glutamate (MSG) in Sprague-Dawley rats. The animals received EEOS (50, 100 and 200 mg/kg) and memantine (MMT, 20 mg/kg) daily for 7 days. On all the 7 days, MSG (2g/kg, i.p.) was administered one hour before drug treatment. The animals were observed for neurobehavioral performance on 1 st , 3 rd , 5 th and 7 th day. Oxidative damage and histopathological analysis were also assessed. EEOS (100 and 200 mg/kg, p.o.) and MMT (20 mg/kg, i.p.) administration significantly improved body weight and attenuated locomotor activity, rotarod performance and footfault test as compared with MSG treated group. In addition, EEOS was found to restore reduced glutathione (GSH), glutathione peroxidase (GPx), glutathione reductase (GR), catalase (CAT), super oxide dismutase (SOD) and Na +-K + ATPase. Conversely, the elevated level of lipid peroxidation and nitrite concentration in MSG treated group was attenuated significantly in EEOS group in comparison to MSG treated group. Histopathological evaluation showed that treatment with EEOS and MMT significantly attenuated neuronal death and increased the density of neurons after MSG treatment. Thus, these findings suggest that EEOS contains rosmarinic acid and ursolic acid in addition to other bioactive principles may have utility in the preventing and/or treating the neurodegenerative diseases and its protective effects may be due to the amelioration of excitotoxicity, oxidative stress, neurological and behavioral alterations. However, further studies are necessary to clearly define mechanism responsible.

Purpose:Oral valproic acid (VPA) used as an anticonvulsant has been shown to improve contrast threshold sensitivities in patients receiving it on long-term. This study aimed to evaluate the efficacy of oral VPA in improving visual function in eyes with advanced stage glaucoma.Methods:In this prospective randomized study, 31 patients (n = 31 eyes) with advanced stage glaucoma (with an intraocular pressure <16 mmHg) in at least one eye received oral VPA 500 mg once a day for 3 months and 33 patients (n = 33 eyes) continued on glaucoma therapy. Patients were followed up at 3 and 12 months (to evaluate the legacy effect of the drug). Blood VPA concentrations were measured at 3 months. Following parameters were assessed at baseline, 3 months and 12 months: log of the minimum angle of resolution (LogMAR) visual acuity, mean deviation on visual fields, and multifocal electroretinogram (ERG).Results:Median LogMar visual acuity in the VPA group improved from 0.3 at baseline to 0.18 and 0.18 at 3 and 12 months, respectively (P < 0.01). In comparison, the median visual acuity in control group at baseline was 0.18 and showed neither worsening nor improvement over 3 and 12 months (P = 0.56). The improvement in VPA group was significant compared to the control group (P < 0.01; Wilcoxon Signed-rank test). An improvement in one line was experienced in 11 out of 31 eyes in the VPA group compared to 1 out of 33 eyes among controls (P = 0.003). No significant improvement was noted in the mean deviation, and the multifocal ERG (Latency and amplitudes) in the VPA-treated patients. The average blood VPA concentration measured at 3 months of therapy was 26 ± 8.9 μg/ml (range 8–55 μg/ml) which is much lower than that achieved during anticonvulsant therapy. None of the patients complained of any adverse effects that required stopping VPA therapy.Conclusion:A 3 months oral VPA therapy results in some improvement in visual acuity in a subgroup of eyes with advanced glaucoma and the effect was seen to persist 9 months after the drug was stopped.