Modulatory potential of Bacopa monnieri against aflatoxin B1 induced biochemical, molecular and histological alterations in rats.

Oxidative injury is concerned with the pathogenesis of several liver injuries, including those from acute liver failure to cirrhosis. This study was designed to explore the antioxidant activity of Bacopa monnieri (BM) on Aflatoxin B1 (AFB1) induced oxidative damage in Wistar albino rats. Aflatoxin B1 treatment (200 µg/kg/day, p.o.) for 28 days induced oxidative injury by a significant alteration in serum liver function test marker enzymes (AST, ALT, ALP, LDH, albumin and bilirubin), inflammatory cytokines (IL-6, IL-10 and TNF-α), thiobarbituric acid reactive substances (TBARS) along with reduction of antioxidant enzymes (GSH, SOD, CAT), GSH cycle enzymes and drug-metabolizing enzymes (AH and AND). Treatment of rats with B. monnieri (20, 30 and 40 mg/kg for 5 days, p.o.) after 28 days of AFB1 intoxication significantly restored these parameters near control in a dose-dependent way. Histopathological examination disclosed extensive hepatic injuries, characterized by cellular necrosis, infiltration, congestion and sinusoidal dilatation in the AFB1-treated group. Treatment with B. monnieri significantly reduced these toxic effects resulting from AFB1. B. monnieriper se group (40 mg/kg) did not show any significant change and proved safe. The cytotoxic activity of B. monnieri was also evaluated on HepG2 cells and showed a good percentage of cytotoxic activity. This finding suggests that B. monnieri protects the liver against oxidative damage caused by AFB1, which aids in the evaluation of the traditional usage of this medicinal plant.

Quercetin ameliorates acute acrylamide induced spleen injury.

Acrylamide is used for industrial and laboratory purposes; it also is produced during cooking of carbohydrate-rich food at high temperature. We investigated the therapeutic potential of quercetin for treatment of acute acrylamide induced injury to the spleen. We used female albino rats treated with acrylamide for 10 days followed by oral administration of quercetin in three doses for 5 days. We observed significantly reduced total body weight, spleen weight, red blood cells, total proteins, superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase, glucose-6-phophate dehydrogenase, reduced glutathione, concentration of serum IgG and IgM after acrylamide induced toxicity compared to controls. We also found that white blood cells, triglycerides, cholesterol and lipid oxidation were increased significantly after acrylamide induced toxicity in rats compared to controls. Histoarchitecture of spleen was affected adversely by acrylamide toxicity. Administration of quercetin ameliorated adverse effects of acrylamide in a dose-dependent manner. Quercetin appears to ameliorate acrylamide induced injury to the spleen by increasing endogenous antioxidants and improving histoarchitecture and immune function.

Oncofertility: Treatment options from bench to bedside.

In recent years, there has been continuous improvement in the treatment and diagnosis of cancer, which has led to a significant improvement in the survival rate of cancer patients. Treatments that include chemotherapy, radiotherapy, surgery, or combined therapy have several side effects that may lead to premature ovarian insufficiency in females or substantial male germ cell loss. Reproductive biologists recommend that all patients who are diagnosed with a malignant tumor must undergo a consultation for fertility protection and preservation. In this review, we discuss the background knowledge, methods, and options for fertility preservation and how these new strategies help oncologists, surgeons, pediatricians, and hematologists, conserve fertility and be aware of the concepts, methods, and importance of fertility guards. This review may aid in the advancement of novel personalized methods for fertility preservation according to patients' conditions.

Ameliorative impact of herbal formulation -Majoon-Dabeed-ul-ward and Sharbat-e-Deenar against CCl4 induced liver toxicity via regulation of antioxidant enzymes and oxidative stress.

Polyherbal Unani formulations have been used in the treatment of liver diseases for a long time. (Ibrahim M, Khaja MN, Aara A, Khan AA, Habeeb MA, Devi YP, Narasu ML, Habibullah CM. Hepatoprotective activity of Sapindus mukorossi and Rheum emodi extracts: in vitro and in vivo studies. World J Gastroenterol. 2008:14:2566-2571.) The aim of the present study was to investigate comparative hepatoprotective potential of Majoon-e-Dabeed-ul-ward (MD) and Sharbat-e-Deenar (SD) against CCl4 induced subchronic hepatic toxicity. In vivo study, albino rats were divided into 5 groups. Group I was control; Group II was experimental control treated with CCl4 (0.15 mL/kg, i.p. for 21 days); Groups III-IV treated with SD (2 mL/kg, p.o.) and MD (1,000 mg/kg, p.o.) for 5 days following CCl4 intoxication as in group 2 respectively; and Group V was positive control treated with silymarin (50 mg/kg, p.o.). In vitro hepatoprotective activity of SD and MD (25, 50, and 100 µg/mL) was assessed by SRB assay and flow cytometry analysis. CCl4 exposure significantly elevated the release of hepatic enzymes i.e. AST, ALT, LDH, and SALP in serum and lipid peroxidation in liver tissue which all these parameters were reversed after SD and MD administration. Therapy for 5 days also normalized the levels of antioxidant enzymes i.e. catalase, SOD, GPx, GR, tissue GSH, and aniline hydroxylase in CCl4 treated group. DNA damage and histological alterations caused by CCl4 were restored towards normal group. In vitro study showed protective effect of SD and MD against CCl4 treated HepG2 cell lines and rat hepatocytes. The results suggested that MD has a significant hepatoprotective potential and regulatory effect on oxidative stress than SD against CCl4 induced hepatotoxicity, and that this effect may be related to its antioxidant activity.

Evidences of the radiofrequency exposure on the antioxidant status, potentially contributing to the inflammatory response and demyelination in rat brain.

Present study exhibited the oxidative potential of microwave radiation (MWR) leading to the neurodegeneration in rats. Wistar rats were exposed at 2100 MHz frequency for 4 h/day, 5 days/week/3 months. Animals were exposed at an estimated specific absorption rate (0.453 W/kg) and power density (8.237 µW/m2). After exposure irradiated group was compared with control group. Results indicated that microwave exposure significantly increased the levels of serological triglycerides and cholesterol. Oxidative stress is observed through alteration of glutathione homeostasis followed by activated inflammatory response further confirmed by pro and anti-inflammatory cytokines in the exposed group. Histopathological assessments and electron microscopic observation confirmed a significant change in the myelination pattern and cellular organelles in the brain of exposed animals. Taking everything into account it can be concluded that chronic exposure of 2100-MHz frequency caused oxidative stress, which leads to neural damage and demyelination and may affect neural communication.

Defensive role of Nigella sativa against antituberculosis drugs induced renal toxicity.

Drug-induced nephrotoxicity is a common problem in clinical medicine and the frequency of drug-related acute and chronic kidney dysfunction worldwide. One of them is anti-tuberculosis (TB) drugs that cause renal function impairment during TB treatment. Medicinal plants contain bioactive compounds that are capable for treating drug or toxin-induced renal disorders. The aim of the present study was to assess the protective effect of the ethanolic extract of Nigella sativa seeds (NS) against anti-TB drugs (ATDs) induced nephrotoxicity in Wistar albino rats. Rats were treated with ATDs for 12weeks (3 alternative days in a week). Supplementation with 125mg NS/kg, p.o. was administered to the experimental rats for 12weeks (3 alternative days in a week considering next day of ATDs treatment). The results demonstrated that NS treatment protected against renal damage induced by ATDs, as evidenced by the reduction in serum urea, creatinine, uric acid, urea nitrogen levels, pro-inflammatory markers (TNF-α and IL-6), whereas improvement in histological tubular and glomerular damage. In addition, NS enhanced the antioxidant enzyme activity (superoxide dismutase and catalase) and decreased the lipid peroxidation and glutathione level in the kidney. In conclusion, NS could reduce chronic nephritis in ATDs treated group through suppressing inflammation and oxidative stress. It suggests that NS can be used as supplementary preventive and protective drug against kidney injury during anti-TB treatment.

Protective efficacy of rutin against acrylamide-induced oxidative stress, biochemical alterations and histopathological lesions in rats.

Acrylamide is a well-known neurotoxicant and carcinogen. Apart from industrial exposure, acrylamide is also found in different food products. The present study deals with in vivo experiment to test the protective effect of rutin against acrylamide induced toxicity in rats. The study was carried out on female rats with exposure of acrylamide at the dose of 38.27 mg/kg body weight, orally for 10 days followed by the therapy of rutin (05, 10, 20 and 40 mg/kg orally), for three consecutive days. All animals were sacrificed after 24 h of last treatment and various biochemical parameters in blood and tissue were investigated. Histopathology of liver, kidney and brain was also done. On administration of acrylamide for 10 days, neurotoxicity was observed in terms of decreased acetylcholinesterase activity and oxidative stress was observed in terms of increased lipid peroxidation, declined level of reduced glutathione, antioxidant enzymes (superoxide dismutase and catalase) in liver, kidney and brain. Acrylamide exposure increased the activities of serum transaminases, lipid profile, bilirubin, urea, uric acid and creatinine in serum indicating damage. Our experimental results conclude that rutin showed remarkable protection against oxidative DNA damage induced by acrylamide, which may be due to its antioxidant potential.

Biomimetic synthesis of silver nanoparticles for treatment of N-Nitrosodiethylamine-induced hepatotoxicity.

The development of bioengineered nanoparticles has attracted considerable universal attention in the field of medical science and disease treatment. Current studies were executed to evaluate the hepatoprotective activity of biosynthesized silver nanoparticles (AgNPs). Their characterization was performed by UV-Visible analysis, fourier transform infrared spectroscopy, transmission electron microscopy (TEM), scanning electron microscope (SEM), and Zeta analyses. In in vivo studies, albino rats (180 ± 10 g) were persuaded with model hepatic toxicant N-nitrosodiethylamine (NDEA) and subsequently cotreated with Morus multicaulis at 100 mg/kg and AgNPs at 100 µg/kg dose. NDEA administration elevates the levels of liver function test biomarkers, which were reinstated to normal by cotreatment of test drugs. The oxidative stress and concentration of drug-metabolizing enzyme increase after induction of toxicant (NDEA), these markers are restored toward normal after cotreatment of nano-drug. Treatments of M. multicaulis extract did not show such significant protection. The NDEA-treated groups showed a significant rise in the level of cytokines (interleukin [IL-6] and IL-10) and reached normal with subsequent treatment with AgNPs. Histopathological studies also exhibited the curative effect of AgNPs in the same manner. Thus current results strongly suggest that biomimetic AgNPs could be used as an effective drug against hepatic alteration.

Oxidative damage in the liver and brain of the rats exposed to frequency-dependent radiofrequency electromagnetic exposure: biochemical and histopathological evidence.

The study aimed to discover a link between the liver and brain's functional status due to frequency dependent-radiofrequency electromagnetic radiation (RF-EMR). Forty Wistar rats were randomly classified as control (sham-exposed) and EMR exposed groups. Animals were exposed to 900, 1800, and 2100 MHz with the specific absorption rate (SAR) 0.434 (W/Kg), 0.433 (W/Kg), and 0.453 (W/Kg) respectively. Animal exposure was limited at 1 h/day, 5 days/week for 1 month with a restricted power density (900 MHz- 11.638 µW/m2, 1800- 11.438 µW/m2 and 2100 MHz frequency- 8.237 µW/m2). Exposure at various frequencies showed a frequency-dependent change in the body weight and hematologic parameters (RBCs, WBCs, platelets, hemoglobin, and hematocrit) as compared with the control group (p ≤ 0.01) (p ≤ 0.001). A significant elevation in serum transaminases and bilirubin, urea, uric acid, and creatinine was noted, whereas albumin significantly decreased after EMR exposure (p ≤ 0.01) (p ≤ 0.001). The blood glucose, lipid peroxidation, triglycerides, and cholesterol were elevated while adenosine triphosphatases, acetylcholinesterase, and tissue antioxidants such as glutathione, superoxide dismutase, catalase, glutathione reductase, glutathione Peroxidase, glutathione-S-transferase, and glucose-6-phosphate dehydrogenases were decreased significantly (p ≤ 0.001). Histopathological observations of the liver showed centrilobular mononuclear cell infiltration and swelling in sinusoidal spaces, while in the brain degenerated pyramidal and Purkinje neurons were seen. Furthermore, Substantial evidence was found that the brain is more susceptible to oxidative mutilation compare to the liver of exposed animals. In conclusion, RF-EMR exposure showed oxidative damage to the liver, increasing the incidence of brain damage in a frequency-dependent manner.HighlightsEMR exposure showed frequency-dependent toxicity.Alterations in blood profile and modifications in the serological markers.Increasing lipid peroxidation indicating membrane damage.Inhibition of acetylcholinesterase activity affecting cholinergic neurotransmission.EMR exposure resulted in the loss of cellular energy and production of excess amounts of ROS thereby altering several antioxidant enzymes.Histopathological evidence of severe degenerative changes in the liver and brain.

A preliminary study on urinary excretion patterns of methylprednisolone after oral and intra-articular administration and effect on endogenous glucocorticosteroids profile.

INTRODUCTION: The use of glucocorticosteroids (GCs) through oral, intravenous, intramuscular, or rectal routes is prohibited in sports. Its use is permitted through inhalation, topical and intra-articular route of administration. Methylprednisolone (MP) is available for use by different routes for anti-inflammatory and immunosuppressive purposes. To discriminate its intake by permitted & forbidden routes, a reporting level of 30 ng/ml is set by World Anti-Doping Agency. The aim of this study was to compare MP's excretion profile following oral & intra-articular administration & to evaluate its effect on endogenous GCs profile. MATERIALS & METHODS: The MP was administered through oral and intra-articular route to different patients & urine samples were collected up to 100 h. The urine samples were hydrolyzed, extracted, and analyzed on Liquid chromatography-mass spectrometry/MS. RESULTS: MP levels in urine exceeded the reporting limit of 30 ng/ml after oral (8 mg) and intra-articular administration (80 mg) routes. After oral intake (8 mg), MP levels exceeded the reporting level up to 24 h. However, after intra-articular injection (80 mg), the MP could be detected above the reporting level up to 80 h. CONCLUSION: The findings reveal that the MP can exceed the reporting level in urine even after administration by permitted route (i.a.). Further analysis of four endogenous GCs (Cortisol, Cortisone, TH Cortisone, and 11-deoxycortisol) showed a decreased excretion following administration of MP by oral & intra-articular routes.

Exposure of Radiofrequency Electromagnetic Radiation on Biochemical and Pathological Alterations.

INTRODUCTION: In the era of globalization, too much dependency on mobile phones is a cause of concern. OBJECTIVE: The present study was designed to evaluate the risk assessment of microwave radiation (MWR) at 1800 MHz frequency and specific absorption rate 0.433 (W/kg) on male Wistar rats. METHODOLOGY: Animals were divided into two groups: the first group is the control group, and the second group was exposed to 1800 MHz radiation for 90 days at 4 h/5 days/week in a month. RESULTS: Chronic exposure of MWR may alter GSH homeostasis due to alteration in various GSH cycle regulating enzymes such as GR, GPx, GST, and G6PDH which showed an imbalance in GSH content and causes an increase in the oxidative stress and release of inflammatory cytokines. A remarkable increase in the DNA damage was seen due to disorganization and pyknosis of neurons in exposed animal's brain when compared with the control group (P ≤ 0.05). There was also a significant decline in AChE level. CONCLUSION: The study concludes that MWR may cause neurochemical and pathophysiological damage by initiating the inflammatory process in various brain regions, especially in hippocampus and cerebral cortex. These effects are further associated with a remarkable elevation in the genotoxicity of neurons with reference to the control group.

Acetaminophen-induced renal toxicity: preventive effect of silver nanoparticles.

Present study was planned to investigate the ameliorative effect of silver nanoparticles (AgNPs) on acetaminophen-induced nephrotoxicity. Our results demonstrate that therapy of AgNPs at three different doses (50, 100 and 150 µg/kg once only) prevented the acetaminophen (2 g/kg once only) induced acute renal toxicity. AgNPs treated animals also show less intensity in the histological alterations in kidneys and corroborating the results of analysis of serum urea and creatinine. In addition, AgNPs therapy prevented the acetaminophen-induced oxidative stress, which was confirmed by the alleviated lipid peroxidation, enhanced renal reduced glutathione content and restored enzymatic activities of superoxide dismutase, catalase and adenosine triphosphatase in kidney. Thus, our results demonstrate a possible protective potential of AgNPs on renal toxicity induced by acetaminophen. This study will definitely lead to the development of therapeutic drug against nephrotoxicity, after further clinical and preclinical studies.

Effect of electromagnetic radiation on redox status, acetylcholine esterase activity and cellular damage contributing to the diminution of the brain working memory in rats.

Behavioral impairments are the most pragmatic outcome of long-term mobile uses but the underlying causes are still poorly understood. Therefore, the Aim of the present study to determine the possible mechanism of mobile induced behavioral alterations by observing redox status, cholinesterase activity, cellular, genotoxic damage and cognitive alterations in rat hippocampus. This study was carried out on 24 male Wistar rats, randomly divided into four groups (n = 6 in each group): group I consisted of sham-exposed (control) rats, group II-IV consisted of rats exposed to microwave radiation (900 MHz) at different time duration 1 h, 2 h, and 4 h respectively for 90 days. After 90 days of exposure, rats were assessing learning ability by using T-Maze. A significantly increased level of malondialdehyde (MDA) with concomitantly depleted levels of superoxide dismutase (SOD), catalase (CAT) and redox enzymes (GSH, GPX, GR, GST, G-6PDH) indicated an exposure of mobile emitted EMR induced oxidative stress by the depleted redox status of brain cells. The depletion in the acetylcholinesterase (AChE) level reveals altered neurotransmission in brain cells. Resultant cellular degeneration was also observed in the radiation-exposed hippocampus. Conclusively, the present study revealed that microwave radiation induces oxidative stress, depleted redox status, and causes DNA damage with the subsequent reduction in working memory in a time-dependent manner. This study provides insight over the associative reciprocity between redox status, cellular degeneration and reduced cholinergic activity, which presumably leads to the behavioral alterations following mobile emitted electromagnetic radiation.

Moderate noise associated oxidative stress with concomitant memory impairment, neuro-inflammation and neurodegeneration.

Noise, a disturbing and unwanted sound is currently being perceived as a widespread environmental stressor. In the present study we investigated the activation of oxidative stress as a mechanism involved in cognitive impairment through changes in neuro-inflammation. Sprague Dawley rats (200-220 â€‹ â€‹g â€‹m) were exposed to moderate (100dB) sound pressure level (SPL) noise daily for 2 â€‹h â€‹s over a period of 15 and 30 days and the consequence on brain regions of hippocampus observed through behavioral studies by Morris Water Maze to assess effects on spatial memory coupled with biochemical evaluation of markers of oxidative stress and inflammation. Further, the underlying mechanism pertaining to apoptosis was investigated by immuno-histological studies through assessment of Caspase-3 and TUNEL assay as well as morphological parameters, namely Nissl bodies in CA1, CA3 and DG regions of hippocampus. Poorer performance in the MWM indicative of decrement in concept formation, attention, working memory, and reference memory was observed on 15 and 30 days of noise exposures. At the cellular level, increased oxidative stress and inflammation was noticed as evinced by elevated levels of TNF-α, IL-6, IL-1α and IFN-γ in both hippocampus and plasma. Exposure to noise also led to a gradual increase in the number of pyknotic and apoptotic neurons together with the increase in DNA fragmentation in hippocampus. Increased levels of inflammatory genes (i.g.) ccl2, ccr5, ifng, il13, il1a, tnfa coupled with decreased levels of bmp2 and il3 genes were found in both the noise exposure groups. Our findings revealed that moderate intensity noise exposure impaired early memory changes in expression of several gene families including genes associated with regulation of transcription, inflammatory response, and, response to oxidative stress.

Mobile phone induced cognitive and neurochemical consequences.

With the rapid advances in technology, extensive use of mobile phones has increased the risk of health problems. This study was performed to find out the effect of mobile phone frequency on male Wistar rats. Animals were divided into two groups (n = 6 in each group). Group one was considered as control and group two (experimental group) was exposed to microwave radiation (2100 MHz) for 4 hours/day (5 days/week) for 3 months. Exposure of microwave radiation frequency showed significant alterations in cholinesterase activity, muscular strength, learning ability and anxiety. MWR exposure was also associated with significant alteration in the oxidative defense system and hippocampus degeneration. Histopathological observations clearly depicted the neural degeneration. Thus, it can be concluded that MWR significantly affects the central nervous system and may lead to many severe illnesses. This study may reveal a platform to understand its toxic effect and can further be used for amendment in current guidelines of mobile radiation.

Role of M.tuberculosis protein Rv2005c in the aminoglycosides resistance.

Tuberculosis is an airborne infectious disease caused by Mycobacterium tuberculosis which threatens the globe. Aminoglycosides {Amikacin (AK) & Kanamycin (KM)} are WHO recommended second-line anti-TB drugs used against the treatment of drug-resistant tuberculosis. Aminoglycosides target the steps of protein translation machinery of M.tuberculosis. Several mechanisms have been put forward to elucidate the phenomena of aminoglycosides resistance but our knowledge is still insufficient. The aim of the study was to understand the involvement of Mycobacterium tuberculosis universal stress protein (Rv2005c) in aminoglycosides resistance and virulence. To establish the relationship of universal stress protein Rv2005c with AK & KM resistance, Rv2005c was cloned, expressed in E.coli BL21 using pQE2 expression vector and antimicrobial drug susceptibility testing (DST) was carried out. STRING-10 was also used to predict the interacting protein partners of Rv2005c. DST showed that the minimum inhibitory concentration of induced recombinant cells (Rv2005c) were five and four folds shifted with AK and KM E-strips, respectively. STRING-10 showed the interacting protein partners of Rv2005c. Overexpression of Rv2005c leads to shifting in MIC which might be signifying its involvement in the survival/resistance of Mycobacteria by inhibiting/modulating the effects of AK and KM released from the E-strips. Interactome also suggests that Rv2005c and its interacting protein partners are cumulatively involved in M.tuberculosis resistance, stresses, and latency.

Attenuation of adverse effects of noise induced hearing loss on adult neurogenesis and memory in rats by intervention with Adenosine A2A receptor agonist.

Hearing loss and cognitive decline are commonly associated with aging and morbidity. Present clinical interest lies in whether peripheral hearing loss promotes cognitive decline and if prophylaxis with selective adenosine receptor agonist CGS21680 effectively mitigates the adverse effects. In the current study, male Sprague Dawley rats weighing 200-250 g m were randomly allocated into three groups: Group 1) rats exposed to 100 dB SPL white noise, 2 h a day for 15 consecutive days, 2) rats supplemented with an adenosine receptor agonist, CGS21680 at 100 µg/kg/day prior to noise exposure and 3) unexposed control rats. Baseline hearing and cognition assessed by auditory brainstem response (ABR) and water maze respectively was undertaken for all the groups. Phalloidin stain and synaptic ribbons count in cochlea, and, Ki67, DCX and NeuN in hippocampus were observed by immunohistochemistry. It was inferred that noise exposed rats showed elevated thresholds of ABR and poorer performances in spatial working memory when compared with controls. On the contrary, CGS21680 administered group exhibited improved ABR and cognitive functions with shorter mean latency and path-length to reach the platform, significant reduction in the noise induced loss of synaptic ribbons count and increased number of Ki67 and doublecortin (DCX) positive cells compared to their noise exposed counterparts. Pharmacologic intervention with selective A2A receptor agonist CGS21680 provided adequate protection from noise by effectively maintaining hearing threshold levels, cell viability in cochlea and hippocampus & functional/intact reference memory.

Phytofabrication of Silver nanoparticles: Novel Drug to overcome hepatocellular ailments.

This study aimed to treat hepatocellular ailments with biologically prepared silver nanoparticle (AgNPs). AgNPs were formulated using Morus alba leaf extract and their synthesis and characterization were determined by UV-visible spectroscopy, Transmission Electron Microscope (TEM), Scanning Electron microscope (SEM), X-ray diffraction (XRD), Fourier transform infrared spectroscopy (FT-IR) and Zeta analysis. In vitro studies on HepG2 cell lines for cytotoxic effect and in vivo studies in a rat model for hepatoprotective effect were carried out using biologically prepared AgNPs as curing agents. Dose response cytotoxicity on hepatic cancer (HepG2) cells was confirmed by 3-(4, 5-dimethyl thiazole-2-yl)-2, 5-diphenyl tetrazolium (MTT) assay. The inhibitory concentrations (IC50) were found to be 20 µg/mL and 80 µg/mL for AgNPs and M. alba leaf extract respectively against HepG2 cells at 24 h incubation. In addition, hepatotoxicity in Wistar rats (180 ±â€¯10 g) was induced by intraperitoneal injection of N-nitrosodiethylamine (NDEA) and were treated with different doses of AgNPs (25, 50, 100 µg/kg). NDEA administration showed a significant rise in the biochemical parameters whereas the levels of enzymic antioxidants were decreased. Obtained results revealed that the elevated levels of Liver Function Test (LFTs) biomarkers were significantly reversed and the antioxidant levels were significantly recouped towards normal after the conjoint treatment of AgNPs in a dose-dependent manner. Thus green synthesized AgNPs showed a promising curing effect on hepatocellular ailments.

Identification of Cross Reactive Antigens of C. botulinum Types A, B, E & F by Immunoproteomic Approach.

Diseases triggered by microorganisms can be controlled by vaccines, which need neutralizing antigens. Hence, it is very crucial to identify extremely efficient immunogens for immune prevention. Botulism, a fatal neuroparalytic disease, is caused by botulinum neurotoxins produced by the anaerobic, Gram-positive spore-forming bacteria, Clostridium botulinum. Food-borne botulism and iatrogenic botulism are caused by botulinum toxin. Wound botulism, infant botulism, and adult intestinal botulism are caused by primarily C. botulinum followed by secondary intoxication. To identify protective antigens, whole cell proteome of C. botulinum type B was separated by two-dimensional gel electrophoresis. 2-D gel of whole cell proteins was probed with hyper immune sera of whole cell proteins of C. botulinum types A, E, and F. Six cross immunoreactive proteins were identified. These immunoreactive proteins will be further tested for developing vaccines and serodiagnostic markers against botulism.

Anthrax lethal toxin (LeTx) neutralization by PA domain specific antisera.

Anthrax associated causalities in humans and animals are implicated mainly due to the action of two exotoxins that are secreted by the bacterium Bacillus antharcis during the infection. These exotoxins comprise of three protein components namely protective antigen (PA), lethal factor (LF) and edema factor (EF). The protective antigen is the common toxin component required to form both lethal toxin (LeTx) and edema toxin (EdTx). The LeTx is formed, when PA combines with LF and EdTx is formed when PA combines with EF. Therapeutic interventions aiming to neutralize these key effectors of anthrax pathology would therefore, provide an effective means to counter the toxicity imposed by the anthrax toxins on the host. The present work describes the lethal toxin neutralization potential of polyclonal antisera developed against the individual domains of the protective antigen component of the anthrax toxin. The individual domains were produced as recombinant proteins in E. coli and validated with peptide mass fingerprinting by MALDI-TOF analysis and corresponding mice polyclonal antisera by western blotting. Each domain specific antibody titre and isotype was ascertained by ELISA. The isotyping revealed the predominance of IgG1 isotype. The toxin neutralizing potential of these domain specific antisera were evaluated by in-vitro cell viability MTT assay, employing J774.1 mouse macrophage cell line against LeTx (0.25 µg ml-1 PA and 0.125 µg ml-1 LF concentrations). Among the four domain specific antisera, the antiserum against PA domain IV could neutralize LeTx with high efficiency. No significant neutralization of LeTx was observed with other domain specific antibodies. Results indicate that antibodies to r-PA domain IV could be explored further as therapeutic anti toxin molecule along with appropriate antibiotic regimens against anthrax.