Effect of Different Bulking Materials and Earthworms Species on Bioremediation Potential of Municipal Sewage Sludge

In present study the efficiency for vermiremediation of municipal sewage sludge (MSS) with different bulking materials such as Cow Dung (CD), Sheep Manure (SM) and Garden Soil (GS) in presence of Eudrilus eugeniae and Eisenia foetida was investigated. The results revealed that interaction of worm species and bulking materials had significant effect on moisture %, EC and Cl- but it was non significant for pH and Organic Carbon (OC). At final stage of vermiremediation OC, EC and Cl- were reduced as compare to initial stage. The highest values for EC (8804 µmohs/cm) and OC (25.63 %), were noted in the treatment SS + CD and no worm species.  While maximum Cl- (1423 ppm) was found in treatment SS + no bulking material and no worm species. The results also indicated that the lowest EC (3424 µmohs/cm) was in treatment SS + GS + Eudrilus eugeniae, OC (13.83 %) was in treatment SS + no bulking material + Eudrilus Eugeniae and Cl- (643.0 ppm) was noted in treatment SS + CD + Eudrilus eugeniae. It is concluded that the effective bioremediation of sewage sludge is possible with cow dung manure or garden soil along with Eudrilus eugeniae or Eisenia foetida. Keywords: bulking, earthworm, remediation, sewage sludge

Amino Acid-Containing Krebs-Henseleit Buffer Protects Rat Liver in a Long-Term Organ Perfusion Model

Background: The liver is vulnerable to the toxicity induced by xenobiotics. On the other hand, it has been found that several endogenously-found amino acids have hepatoprotective properties. The current study was designed to evaluate the effect of taurine, glycine, and histidine on the liver function in an ex vivo model of prolonged organ perfusion. Methods: Rat liver was isolated and perfused with a hemoglobin- and albumin-free Krebs-Henseleit buffer (KBH). Liver injury biomarkers were monitored at scheduled time intervals. Results: The perfusate level of lactate dehydrogenase (LDH), alanine aminotransferase (ALT), aspartate aminotransferase (AST), and the potassium ion (K+) were gradually increased in control (Only KBH) group. The histopathological evaluation also revealed significant necrosis, sinusoidal dilation, and pyknosis in control liver. Moreover, significant increase in lipid peroxidation and depletion of hepatic glutathione stores were detected in the control group. It was found that taurine (5, 10 and 20 mM) and glycine (5, 10 and 20 mM)-containing KBH buffer significantly decreased the perfusate level of liver injury biomarkers. Furthermore, lower liver tissue pathological changes, decreased lipid peroxidation, and higher glutathione content was detected in amino acid-treated groups. Histidine administration showed no significant protective effect on liver injury in the current study. On the other hand, combination amino acid administration (glycine and taurine) showed a better hepatoprotective profile. Conclusion: The data obtained from the current study might help to provide safe hepatoprotective agents against xenobiotics-induced hepatotoxicity or preserve liver functionality outside the body

Boldine Supplementation Regulates Mitochondrial Function and Oxidative Stress in a Rat Model of Hepatotoxicity

Background: The xenobiotics-induced liver injury is a clinical complication. Hence, finding new hepatoprotective strategies has clinical value. Oxidative stress and its subsequent complications are major mechanisms involved in xenobiotics-induced hepatotoxicity. Boldine is one of the most potent antioxidant molecules widely investigated for its protective properties in different experimental models. In the current study, the hepatoprotective properties of boldine and its potential mechanisms of hepatoprotection have been investigated. Methods: Rats received thioacetamide (TAA; 200 mg/kg, i.p) as a model of acute liver injury. Boldine (5, 10, 1nd 20 mg/kg; 24 hours intervals; oral) was administered as the hepatoprotective agent. Results: Liver injury was evident in TAA-treated animals (48 hours after TAA exposure) as a severe increase in serum level of liver injury biomarkers and histopathological alterations. Moreover, markers of oxidative stress were increased in liver tissue of TAA-treated rats. Assessment of mitochondrial indices of functionality revealed a significant decrease in mitochondrial dehydrogenases activity, the collapse of mitochondrial membrane potential, mitochondrial swelling and depletion of ATP content. It was found that boldine supplementation mitigated liver tissue markers of oxidative stress and improved mitochondrial indices of functionality in TAA-treated animals. Conclusion: The hepatoprotective properties of boldine might primarily rely on antioxidant and mitochondria protecting effects of this alkaloid

The Hepatoprotective Role of Thiol Reductants against Mitoxantrone-Induced Liver Injury

Mitoxantrone is anthracycline antibiotic highly effective against various human cancers. Hepatotoxicity is associated with mitoxantrone administration. On the other hand, there is no effective therapeutic option against chemotherapy-induced liver injury. The current investigation was designed to evaluate the effect of thiol reductants on mitoxantrone-induced liver injury in two experimental models. As an ex vivo model, isolated rat liver was exposed to increasing concentrations of mitoxantrone (100, 250, 750, and 1000 µM) alone or in combination with thiol-reductants (Dithiothreitol; DTT, and N-acetyl cysteine; NAC). In addition, rats (in vivo) received mitoxantrone (2.5 mg/kg, i.p, at days 1, 10, and 20), NAC (100 and 300 mg/kg/day, i.p, for 20 consecutive days) and DTT (15 and 30 mg/kg/day, i.p, for 20 consecutive days), then liver and serum pathological changes were monitored. Mitoxantrone-induced liver injury was evident in both ex vivo and in vivo experiments as assessed by pathological changes in biomarkers of liver injury, along with tissue histopathological changes. Furthermore, an increase in liver tissue markers of oxidative stress was detected in the mitoxantrone-treated group. It was found that thiol reductants significantly mitigated mitoxantrone hepatotoxicity. The data indicate that thiol reductants might serve as hepatoprotective agents against chemotherapy-induced liver injury.</p

The Effect of Mesenchymal Stem Cells on the Expression of IDOand Qa2 Molecules in Dendritic Cells

Purpose: Mesenchymal stem cells (MSCs) have been shown to reduce the activity of immunecells, including dendritic cells (DCs). But the exact mechanism of mesenchymal inhibitionof DCs is still unknown. In this study, the effect of mesenchymal cells on the expression ofindoleamine dioxygenase (IDO) and Qa2 molecules in DCs was evaluated.Methods: MSCs and DCs were respectively isolated from the bone marrow and spleen of BALB/cmice. Then DCs were co-cultured with MSCs in the present and absence of lipopolysaccharides(LPS). Then the expression of mRNA and protein of IDO and Qa2 molecules were investigatedin DCs that were treated with MSCs.Results: The expression of IDO and Qa2 mRNA in DCs that were treated with MSCs did notsignificantly differ from the control group. The expression of IDO protein in DCs that were coculturedwith MSCs (in 1:10 and 1:50 ratios) in absence of LPS was increased, although theywere not statistically significant (P values: 0.24 and 0.18, respectively). The expression of Qa2protein in DCs that were co-cultured with MSCs (in 1:10 and 1:50 ratios) in presence of LPS wasincreased, although they were not statistically significant (P-values: 0.09 and 0.33, respectively).Conclusion: Our results denied the possibility that MSCs led to the induction of tolerogenic DCsby increasing the expression of the IDO and Qa2 immunomodulatory molecules

Carnosine Supplementation Mitigates Brain Tissue Markers of Oxidative Stress in a Rat Model of Fulminant Hepatic Failure

Fulminant hepatic failure is a deleterious clinical complication, which leads to hyperammonemia. Ammonia is a noxious neurotoxic agent, which affects brain tissue through different mechanisms. On the other hand, it is well-known that oxidative stress and its consequences play a major role in the pathogenesis of ammonia-induced brain injury. Carnosine is a dipeptide abundantly found in the human central nervous system (CNS). This peptide is widely investigated for its neuroprotective properties. The current study aimed to evaluate the effect of carnosine supplementation on oxidative stress markers in the brain tissue of a rat model of fulminant hepatic failure and hyperammonemia. Animals received thioacetamide (400 mg/kg, i.p, for three consecutive days at 24-hr intervals) as a model of acute liver failure and hyperammonemia. Several serum biochemical parameters, in addition to plasma and brain ammonia level, were monitored. On the other hand, brain tissue markers of oxidative stress including reactive oxygen species (ROS) formation, lipid peroxidation, tissue glutathione content, and total antioxidant capacity were measured. It was found that plasma and brain ammonia was increased, and serum markers of liver injury were significantly elevated in the thioacetamide-treated group. On the other hand, an increase in markers of oxidative stress, including ROS formation, lipid peroxidation, glutathione depletion, and decreased tissue antioxidant capacity, was evident in the brain of thioacetamide-treated animals. It was found that carnosine supplementation (250, 500, and 1000 mg/kg) decreased serum markers of liver injury, mitigated brain, and plasma ammonia level, and alleviated brain tissue markers of oxidative stress. These data suggest carnosine as a potential neuroprotective agent with therapeutic capability against ammonia-induced CNS injury.</p

Taurine Alleviates Brain Tissue Markers of Oxidative Stress in a Rat Model of Hepatic Encephalopathy

Hepatic encephalopathy (HE) is a serious clinical complication, which could lead to coma and death if not appropriately managed. There is agreement on the predominant role of ammonia in the etiology of HE. Brain is one of the most critical organs affected by ammonia. The critical role of oxidative stress and its consequences in the pathogenesis of ammonia-induced brain injury have been revealed before. On the other hand, there is no promising therapeutic option against ammonia neurotoxicity. Taurine is one of the most abundant amino acids in the human body. Several pharmacological roles including brain protecting properties have been attributed to this amino acid. The current study was designed to evaluate the role of taurine supplementation on HE-induced oxidative stress in the brain tissue. Animals received thioacetamide (400 mg/kg, i.p, for three consecutive days at 24-hr intervals) as a model of acute liver failure and hyperammonemia. Several serum biochemical parameters, in addition to plasma and brain ammonia level, were monitored. Moreover, markers of oxidative stress in the brain of hyperammonemic animals were assessed. It was found that plasma and brain ammonia was increased, and serum markers of liver injury were significantly elevated in the thioacetamide-treated group. On the other hand, an increase in markers of oxidative stress, including reactive oxygen species formation, lipid peroxidation, glutathione depletion, and decreased tissue antioxidant capacity, was detected in the brain tissue of thioacetamide-treated animals. It was found that taurine treatment (250, 500, and 1000 mg/kg, i.p) alleviated brain tissue markers of oxidative stress and decreased serum biomarkers of liver injury. Furthermore, lower plasma and brain ammonia were detected in taurine-treated animals. These data suggest taurine as a potential protective agent with therapeutic capability against HE-associated central nervous system complications.</p

Investigation of nitrate and nitrite concentration and other physicochemical parameters of drinking water sources in Saveh city during the year of 2018

Abstract   Background and Purpose:Qualitative parameters of drinking water such as concentration of nitrate, nitrite, sulfate, total soluble solids, sodium, magnesium, fluoride, total hardness and electrical conductivity can play an important role in groundwater resources and are mainly related to agriculture, waste disposal areas and sewage. The aim of this study was to determine these parameters in drinking groundwater resource of Saveh city using Geographic Information System during the year of 2018 and investigation of contaminant’s in the region’s aquifer. Materials and Methods:This research is a descriptive-analytic study. 120 samples of water from 12 drinking water wells were prepared in spring and two times in the morning and afternoon in different parts of the city of Saveh. The quality parameters of drinking water, including concentration of nitrate, nitrite, sulfate, total soluble solids, sodium, magnesium, fluoride, total hardness and electrical conductivity were entered into the GIS software and stored in a database and then processed by the information system software, color mapping was prepared and geographical maps (GIS) were mapped to qualitative status. Also, reverse interpolation was used to estimate the conditions of the whole region. Findings:The average concentration of chlorine, sulfate, electrical conductivity, total soluble solids, total hardness and sodium exceeds the permissible limits, and the non-qualitative water conditions are quite evident. Also, the amount of two magnesium and sulfate ions was above the standard 1053. It should be kept in mind that the high levels of these two ions can interfere with the digestive system. Fluoride and nitrate levels were also acceptable range in all areas. Conclusion:The highest deviation level from 1053 standard was for total soluble solids, sodium, magnesium, and sulfate. It is better to consider a comprehensive program to solve the problem, including use of nanotechnology, filtering or ion exchange

Dexamethasone Blunts Lung Inflammation in Cholestatic Mice

Cholestasis/cirrhosis is a multifaceted clinical complication that influences many organs, including the liver, kidney, heart, skeletal muscle, and lung. Cirrhosis-associated lung injury could lead to severe and lethal consequences, including acute respiratory syndrome and patient dearth. Unfortunately, there is no specific pharmacological intervention to manage cholestasis-induced lung injury. It has been revealed that severe inflammation and its associated complications, such as oxidative stress, are involved in the pathogenesis of cholestasis-associated pulmonary damage. The current study was designed to evaluate the role of dexamethasone (DXM) on lung inflammation in cholestatic mice. For this purpose, bile duct ligated (BDL) mice received DXM (1 and 2.5 mg/kg, i.p, 2 times/week) for 14 days. On day 15, the bronchoalveolar lavage fluid (BALF) was prepared. Several markers, including inflammatory cell infiltration, TNF-α, and IgG, were assessed in the BALF of BDL animals. Significant infiltration of inflammatory cells along with increased TNF-α and IgG were detected in the BALF of BDL mice (14 days after surgery). Moreover, significant ROS formation, glutathione depletion, lipid peroxidation, and protein carbonylation were evident in the lung tissue of the BDL group. It was found that DXM (1 and 2.5 mg/kg) significantly blunted inflammation and oxidative stress in the lung of cholestatic mice. Moreover, lung tissue histopathological changes, including inflammatory cell infiltration, were significantly mitigated in DXM-treated mice. These data offer the potential therapeutic effects of DXM against cholestasis-related complications. Therefore, patients with cholestasis-induced lung injury might benefit from repurposing DXM in clinical settings