Adenosine Triphosphatase Activity Research Articles

Cancer on motors: How kinesins drive prostate cancer progression?

Prostate cancer causes numerous male deaths annually. Although great progress has been made in the diagnosis and treatment of prostate cancer during the past several decades, much about this disease remains unknown, especially its pathobiology. The kinesin superfamily is a pivotal group of motor proteins, that contains a microtubule-based motor domain and features an adenosine triphosphatase activity and motility characteristics. Large-scale sequencing analyses based on clinical samples and animal models have shown that several members of the kinesin family are dysregulated in prostate cancer. Abnormal expression of kinesins could be linked to uncontrolled cell growth, inhibited apoptosis and increased metastasis ability. Additionally, kinesins may be implicated in chemotherapy resistance and escape immunologic cytotoxicity, which creates a barrier to cancer treatment. Here we cover the recent advances in understanding how kinesins may drive prostate cancer progression and how targeting their function may be a therapeutic strategy. A better understanding of kinesins in prostate cancer tumorigenesis may be pivotal for improving disease outcomes in prostate cancer patients.

A four-in-one multifunctional self-assembly hydrogel composed of natural drugs for repairing myocardial infarction

To meet the multiple demands of myocardial repair, it would be a novel strategy for myocardial repair if multiple drugs could be constructed into an integrated multifunctional drug formulation. In this study, four drugs with different functions (thioctic acid with antioxidant effects, quercetin with anti-inflammatory and antioxidant effects, arginine with pro-angiogenic effects, and Mn2+ with imaging functions) were selected to construct a four-in-one injectable hydrogel (thioctic acid-arginine-quercetin-Mn2+) through chemical bonding and supramolecular interactions. First, thioctic acid polymerized to a redox-sensitive degradable polymer—poly(thioctic acid) containing disulfide bonds in the main chains through ring-opening polymerization. Quercetin was conjugated to the main chain of the poly(thioctic acid) molecules via thiyl radical-polyphenol Michael addition. Arginine cross-linked the carboxyl groups side chains of the poly(thioctic acid) molecules through hydrogen bonding. Mn2+ further cross-linked the carboxyl groups' side chains of the poly(thioctic acid) molecules through ionic bonding. The hydrogel has antioxidant properties, promotes neovascularization, inhibits inflammatory, improves intracellular Ca2+ overload and mitochondrial dysfunction, protects adenosine triphosphatase (ATPase) activity, and maintains intracellular energy supply, which can reduce the size of myocardial infarcts, and improves cardiac function. This construction method of preparing integrated multifunctional hydrogels from natural drugs will provide a new therapeutic strategy for myocardial repair.

Acidification of α-granules in megakaryocytes by vacuolar-type adenosine triphosphatase is essential for organelle biogenesis

BackgroundPlatelets coordinate blood coagulation at sites of vascular injury and play fundamental roles in a wide variety of (patho)physiological processes. Key to many platelet functions is the transport and secretion of proteins packaged within α-granules, organelles produced by platelet precursor megakaryocytes. Prominent among α-granule cargo are fibrinogen endocytosed from plasma and endogenously synthesized von Willebrand factor. These and other proteins are known to require acidic pH for stable packaging. Luminal acidity has been confirmed for mature α-granules isolated from platelets, but direct measurement of megakaryocyte granule acidity has not been reported. ObjectivesTo determine the luminal pH of α-granules and their precursors in megakaryocytes and assess the requirement of vacuolar-type adenosine triphosphatase (V-ATPase) activity to establish and maintain the luminal acidity and integrity of these organelles. ResultsUsing cresyl violet staining, we show that most of the acidic granules detected in megakaryocytes appear to be α-granules/precursors. Endocytosis of fibrinogen tagged with the pH-sensitive fluorescent dye fluorescein isothiocyanate was used to load a subset of these organelles, and ratiometric fluorescence analysis established a median luminal pH of 5.2 (IQR, 5.0-5.5). Inhibition of megakaryocyte V-ATPase activity led to enlargement of cargo-containing compartments detected by fluorescence microscopy and electron microscopy. ConclusionThese observations reveal that V-ATPase activity is required to establish and maintain a luminal acidic pH in megakaryocyte α-granules/precursors, confirming its importance for stable packaging of cargo proteins such as von Willebrand factor.

Research Progress on the NSP10 Protein of Porcine Reproductive and Respiratory Syndrome Virus.

Porcine reproductive and respiratory syndrome (PRRS) is a highly contagious and pathogenic infectious disease caused by the porcine reproductive and respiratory syndrome virus (PRRSV). It manifests as reproductive disorders in sows and respiratory disorders in piglets. PRRSV infects swine herds with symptoms such as abortions, stillbirths, and mummified fetuses in gestating sows. Piglets mainly experience abdominal respiration and respiratory symptoms. To date, the prevention of PRRS relies primarily on vaccination and the implementation of various preventive and control measures. Swine deaths caused by PRRS have resulted in significant economic losses to the pig industry worldwide. Non-structural protein 10 (NSP10) has helicase and adenosine triphosphatase (ATPase) activities that unwind DNA and RNA and play important roles in viral replication and transcription. Hence, it can be potentially used to develop novel reagents for the detection of PPRSV. This article reviews genetic variations, interaction with viral and host proteins, effects on PRRSV replication, immunomodulation, apoptosis, and viral virulence of NSP10, with the aim of providing a theoretical basis for the prevention and control of PRRS and drug development in the future.

Protective effects of myricetin and morin on neurological damage in Aβ1–42/Al3+ -induced Alzheimer’s disease model of rats

Alzheimer's disease (AD) is a degenerative neurological disorder with unclear pathogenesis. Single-target drugs have very limited efficacy in treating AD, but synthetic multi-target drugs have poor efficacy and safety. Therefore, finding suitable natural multi-target drugs against AD is of great interest for research studies. We chose two flavonols, myricetin and morin, for the relevant study. In this study, we used microinjection of Aβ1–42 oligomers into the CA1 region of rat hippocampus, combined with gavage of Aluminum chloride hexahydrate (AlCl3·6H2O) solution to establish AD rat models, and myricetin and morin were selected as intervening drugs to explore the protective effects against neurological impairment. Experimental results showed that myricetin or morin could reduce the production of Aβ, Tubulin-associated unit (Tau), and Phosphorylated tubulin-associated unit (p-Tau), down-regulate the expression of relevant inflammatory factors, reduce hippocampal cell apoptosis in rats. There was a significant increase in the activity of adenosine triphosphatase, catalase, total superoxide dismutase, and the content of glutathione in the brain tissue. However, the content of malondialdehyde, inducible nitric oxide synthase, and the activity of acetylcholinesterase were decreased in the brain tissue. These two flavonols can regulate the imbalance of monoamine and amino acid neurotransmitter levels. In conclusion, Myricetin or morin can effectively improve learning and memory dysfunction in AD rats induced by Aβ1–42/Al3+ through anti-oxidative stress and anti-apoptotic features.

Astaxanthin activates the Nrf2/Keap1/HO-1 pathway to inhibit oxidative stress and ferroptosis, reducing triphenyl phosphate (TPhP)-induced neurodevelopmental toxicity

Triphenyl phosphate (TPhP) serves as a major organophosphorus flame retardant, and its induced neurodevelopmental toxicity has attracted widespread attention, but the mechanism remains unclear. In this study, we involved zebrafish to explore the new mechanism of TPhP inducing oxidative stress and ferroptosis to promote neurodevelopmental toxicity. The results suggested that TPhP affected the embryonic development, reduced the number of new neurons, and led to abnormal neural behavior in zebrafish larvae. TPhP also induced ROS accumulation, activated the antioxidant defense signal Nrf2 and Keap1, and significantly changed the activities of Acetylcholinesterase (AChE), Adenosine triphosphatase (ATPase) and glutathione S-transferase (GST). In addition, TPhP induced ferroptosis in zebrafish, which was reflected in the increase of Fe2+ content, the abnormal expression of GPX4 protein and genes related to iron metabolism (gpx4a, slc7a11, acsl4b, tfa, slc40a1, fth1b, tfr2, tfr1a, tfr1b and ncoa4). Astaxanthin intervention specifically inhibited ROS levels, and reversed SLC7A11 and GPX4 expression levels and Fe2+ metabolism thus alleviating ferroptosis induced by TPhP. Astaxanthin also partially reversed the activity of AChE, GST and the expression of neurodevelopmental-related genes (gap43, gfap, neurog1 and syn2a), so as to partially rescue the embryonic developmental abnormalities and motor behavior disorders induced by TPhP. More interestingly, the expression of mitochondrial apoptosis-related protein BAX, anti-apoptotic protein BCL-2, Caspase3 and Caspase9 was significantly altered in the TPhP exposed group, which could be also reversed by Astaxanthin intervention. In summary, our results suggested that TPhP exposure can induce oxidative stress and ferroptosis, thereby causing neurodevelopment toxicity to zebrafish, while Astaxanthin can partially reverse oxidative stress and reduce the neurodevelopmental toxicity of zebrafish larvae by activating Nrf2/Keap1/HO-1 signaling pathway.

The inflammatory injury of porcine small intestinal epithelial cells induced by deoxynivalenol is related to the decrease in glucose transport.

The present study aimed to investigate the effects of deoxynivalenol (DON) stimulation on inflammatory injury and the expression of the glucose transporters sodium-dependent glucose transporter 1 (SGLT1) and glucose transporter protein 2 (GLU2) in porcine small intestinal epithelial cells (IPEC-J2). Additionally, the study aimed to provide initial insights into the connection between the expression of glucose transporters and the inflammatory injury of IPEC-J2 cells. DON concentration and DON treatment time were determined using the CCK‑8 assay. Accordingly, 1.0 µg/mL DON and treatment for 24h were chosen for subsequent experiments. Then IPEC-J2 cells were treated without DON (CON, N = 6) or with 1 μg/mL DON (DON, N = 6). Lactate dehydrogenase (LDH) content, apoptosis rate, and proinflammatory cytokines including interleukin (IL)-1β, Il-6, and tumor necrosis factor α (TNF-α) were measured. Additionally, the expression of AMP-activated protein kinase α1 (AMPK-α1), the content of glucose, intestinal alkaline phosphatase (AKP), and sodium/potassium-transporting adenosine triphosphatase (Na+/K+-ATPase) activity, and the expression of SGLT1 and GLU2 of IPEC-J2 cells were also analyzed. The results showed that DON exposure significantly increased LDH release and apoptosis rate of IPEC-J2 cells. Stimulation with DON resulted in significant cellular inflammatory damage, as evidenced by a significant increase in proinflammatory cytokines (IL-1β, IL-6, and TNF-α). Additionally, DON caused damage to the glucose absorption capacity of IPEC-J2 cells, indicated by decreased levels of glucose content, AKP activity, Na+/K+-ATPase activity, AMPK-α1 protein expression, and SGLT1 expression. Correlation analysis revealed that glucose absorption capacity was negatively correlated with cell inflammatory cytokines. Based on the findings of this study, it can be preliminarily concluded that the cell inflammatory damage caused by DON may be associated with decreased glucose absorption.

Antibacterial Activity and Mechanism of Polygonatum sibiricum Extract Against Bacillus cereus and Its Application in Pasteurized Milk.

The purpose of this study was to reveal the antibacterial activity and mechanism of Polygonatum sibiricum extract (PSE) against Bacillus cereus and further analyze the application of PSE in pasteurized milk (PM). The minimum inhibitory concentration (MIC) and minimum bactericidal concentration (MBC) values and growth curve analysis were used to evaluate the antibacterial activity of PSE against B. cereus. The changes in contents of intracellular adenosine 5'-triphosphate (ATP) and reactive oxygen species (ROS), activities of β-galactosidase, adenosine triphosphatase (ATPase) and alkaline phosphatase (AKP), cell membrane potential, protein and nucleic acid leakage, and cell morphology were used to reveal the antibacterial mechanism. The effects of PSE on viable count and sensory evaluation of PM during storage were analyzed. The results showed that the MIC and MBC values of PSE against B. cereus were 2 and 4 mg/mL, respectively. Growth curve analysis showed that PSE with a concentration of 2 MIC could completely inhibit the growth of B. cereus. After treatments with PSE, the levels of intracellular ATP and ROS, and activities of β-galactosidase, ATPase and AKP of B. cereus were significantly reduced (p < 0.05). Cell membrane was depolarized, amounts of protein and nucleic acid leakage were significantly increased (p < 0.05), and cell morphology was destroyed. Furthermore, PSE significantly reduced the viable count of B. cereus in PM and improved the sensory quality of PM during storage (p < 0.05). Together, our findings suggested that PSE had the desired effect as a natural preservative applied in PM.

Structures of the P. aeruginosa FleQ-FleN master regulators reveal large-scale conformational switching in motility and biofilm control.

Pseudomonas aeruginosa can cause a wide array of chronic and acute infections associated with its ability to rapidly switch between planktonic, biofilm, and dispersed lifestyles, each with a specific arsenal for bacterial survival and virulence. At the cellular level, many of the physiological transitions are orchestrated by the intracellular second messenger c-di-GMP and its receptor-effector FleQ. A bacterial enhancer binding protein, FleQ acts as a master regulator of both flagellar motility and adherence factor secretion and uses remarkably different transcription activation mechanisms depending on its dinucleotide loading state, adenosine triphosphatase (ATPase) activity, interactions with polymerase sigma (σ) factors, and complexation with a second ATPase, FleN. How the FleQ-FleN tandem can exert diverse effects through recognition of a conserved FleQ binding consensus has remained enigmatic. Here, we provide cryogenic electron microscopy (cryo-EM) structures of both c-di-GMP-bound and c-di-GMP-free FleQ-FleN complexes which deepen our understanding of the proteins' (di)nucleotide-dependent conformational switching and fine-tuned roles in gene expression regulation.

Effect of Sublethal Concentrations of Nuvan on Enzymatic Profile of &lt;I&gt;Labeo rohita &lt;/I&gt;(ham.)

Toxic effects of sublethal concentrations of nuvan on acid phosphatase (ACP), alkaline phosphatase (ALP), adenosine triphosphatase (ATPase), succinic dehydrogenase (SDH), lactic dehydrogenase (LDH) and acetyl cholinestrase (AChE) activities were studied in fingerlings of Labeo rohita. Two sublethal concentrations i.e. 10.3 mg/I and 2.06 mg/l were selected basing on the LCso value of nuvan in rohu for this experiment continuing for a period of 45 days. Sublethal exposures at two concentrations reduced the brain AChE, and brain, liver and kidney LDH and ATPase (P &lt; 0.05) over a period of 45 days. The reduction of SDH was detected in all the organs examined except brain on 30 day at 2.06 mg/I. While ALP and AChE activities of brain were decreased, the ACP activity was increased.

Exogenous methyl jasmonate combined with Ca2+ promote resveratrol biosynthesis and stabilize sprout growth for the production of resveratrol-rich peanut sprouts

Promoting resveratrol accumulation in plants and utilizing resveratrol-rich plants as raw materials for the development of functional foods is a promising development direction. The effects of methyl jasmonate (MeJA), in combination with CaCl2 and Ca2+ inhibitors, on physiological metabolism and resveratrol enrichment of peanut sprouts were investigated. MeJA combined with CaCl2 increased Ca2+ content, calmodulin content, and Ca2+- adenosine triphosphatase activity, as well as upregulated calcium-binding proteinase expression levels. Treatment with MeJA plus CaCl2 significantly increased peroxidase and superoxide dismutase activities and antioxidant capacities, significantly decreased the content of malondialdehyde and hydrogen peroxide, which resulted in a significantly increased in sprout length and fresh weight, and alleviated the inhibition of sprout growth. MeJA plus CaCl2 significantly increased the activities of phenylalanine ammonia-lyase and 4-coumarate coenzyme A ligase and upregulated the expression levels of phenylalanine ammonia-lyase, cinnamic acid 4-hydroxylase, and resveratrol synthase, thus significantly increasing resveratrol content. However, MeJA combined with Ca2+ antagonists reversed these effects. These results indicate that MeJA interacts with Ca2+ to promote resveratrol synthesis in peanut sprouts and to improve sprout stress tolerances.

Alternative relay regulates the adenosine triphosphatase activity of Locusta migratoria striated muscle myosin.

Locust (Locusta migratoria) has a single striated muscle myosin heavy chain (Mhc) gene, which contains 5 clusters of alternative exclusive exons and 1 differently included penultimate exon. The alternative exons of Mhc gene encode 4 distinct regions in the myosin motor domain, that is, the N-terminal SH3-like domain, one lip of the nucleotide-binding pocket, the relay, and the converter. Here, we investigated the role of the alternative regions on the motor function of locust muscle myosin. Using Sf9-baculovirus protein expression system, we expressed and purified 5 isoforms of the locust muscle myosin heavy meromyosin (HMM), including the major isoform in the thorax dorsal longitudinal flight muscle (FL1) and 4 isoforms expressed in the abdominal intersegmental muscle (AB1 to AB4). Among these 5 HMMs, FL1-HMM displayed the highest level of actin-activated adenosine triphosphatase (ATPase) activity (hereafter referred as ATPase activity). To identify the alternative region(s) responsible for the elevated ATPase activity of FL1-HMM, we produced a number of chimeras of FL1-HMM and AB4-HMM. Substitution with the relay of AB4-HMM (encoded by exon-14c) substantially decreased the ATPase activity of FL1-HMM, and conversely, the relay of FL1-HMM (encoded by exon-14a) enhanced the ATPase activity of AB4-HMM. Mutagenesis showed that the exon-14a-encoded residues Gly474 and Asn509 are responsible for the elevated ATPase activity of FL1-HMM. Those results indicate that the alternative relay encoded by exon-14a/c play a key role in regulating the ATPase activity of FL1-HMM and AB4-HMM.

Stress of cupric ion and oxytetracycline in Chlorella vulgaris cultured in swine wastewater

Chlorella culturing has the advantages in treatment of wastewater including swine wastewater from anaerobic digesters due to the product of biolipids and the uptake of carbon dioxide. However, there often exist high concentrations of antibiotics and heavy metals in swine wastewater which could be toxic to chlorella and harmful to the biological systems. This study examined the stress of cupric ion and oxytetracycline (OTC) at various concentrations on the nutrient removal and biomass growth in Chlorella vulgaris culturing in swine wastewater from anaerobic digesters, and its biochemical responses were also studied. Results showed that dynamic hormesis of either OTC concentration or cupric ion one on Chlorella vulgaris were confirmed separately, and the presence of OTC not only did not limit biomass growth and lipids content of Chlorella vulgaris but also could mitigate the toxicity of cupric ion on Chlorella vulgaris in combined stress of Cu2+ and OTC. Extracellular polymeric substances (EPS) of Chlorella vulgaris were used to explain the mechanisms of stress for the first time. The content of proteins and carbohydrates in EPS increased, and the fluorescence spectrum intensity of tightly-bound EPS (TB-EPS) of Chlorella vulgaris decreased with increasing concentration of stress because Cu2+ and OTC may be chelated with proteins of TB-EPS to form non-fluorescent characteristic chelates. The low concentration of Cu2+ (≤1.0 mg/L) could enhance the protein content and promote the activity of superoxide dismutase (SOD) while these parameters were decreased drastically under 2.0 mg/L of Cu2+. The activity of adenosine triphosphatase (ATPase) and glutathione (GSH) enhanced with the increase of OTC concentration under combined stress. This study helps to comprehend the impact mechanisms of stress on Chlorella vulgaris and provides a novel strategy to improve the stability of microalgae systems for wastewater treatment.

Cognitive effects of thalamostriatal degeneration are ameliorated by normalizing striatal cholinergic activity.

The loss of neurons in parafascicular thalamus (Pf) and their inputs to dorsomedial striatum (DMS) in Lewy body disease (LBD) and Parkinson's disease dementia (PDD) have been linked to the effects of neuroinflammation. We found that, in rats, these inputs were necessary for both the function of striatal cholinergic interneurons (CINs) and the flexible encoding of the action-outcome (AO) associations necessary for goal-directed action, producing a burst-pause pattern of CIN firing but only during the remapping elicited by a shift in AO contingency. Neuroinflammation in the Pf abolished these changes in CIN activity and goal-directed control after the shift in contingency. However, both effects were rescued by either the peripheral or the intra-DMS administration of selegiline, a monoamine oxidase B inhibitor that we found also enhances adenosine triphosphatase activity in CINs. These findings suggest a potential treatment for the cognitive deficits associated with neuroinflammation affecting the function of the Pf and related structures.

Antibacterial characteristics of allyl methyl disulfide and dimethyl trisulfide of Allium tenuissimum flower essential oil against Escherichia coli O157:H7

The aim of this study was to compare the antibacterial properties of allyl methyl disulfide and dimethyl trisulfide with the chemical compositions of Allium tenuissimum flower essential oil against Escherichia coli O157:H7. Allium tenuissimum flower essential oil was extracted from fresh Allium tenuissimum flower by hydro-distillation method. Its antibacterial activities against Escherichia coli O157:H7, Staphylococcus aureus and Listeria monocytogenes were determined by diameters of the inhibition zone. Escherichia coli O157:H7 treated with the essential oil had the largest diameter of the inhibition zone (15.2 mm) among the three strains. Allyl methyl disulfide and dimethyl trisulfide were two main compounds of the essential oil, as analyzed by gas chromatography-mass spectrometry. The antibacterial characteristics of these two compounds against Escherichia coli O157:H7 were evaluated by minimum inhibitory and bactericidal concentrations, morphologies, cytomembrane destructions, biomacromolecule contents, and metabolic enzyme activities. Minimum inhibitory concentrations of allyl methyl disulfide and dimethyl trisulfide were both 0.7 mg/mL, and minimum bactericidal concentrations of these two compounds were both 1.4 mg/mL. The images of atomic force microscopy exhibited that the surface structures and cytomembranes of Escherichia coli O157:H7 cells were rigorously damaged by 1.4 mg/mL of allyl methyl disulfide and dimethyl trisulfide, leading to the change of β-galactosidases and the leakage of cellular nucleic acids from the bacterial cells. Moreover, the intensities of deoxyribonucleic acid and protein bands of the bacterial cells were significantly decreased after treated with these two compounds at 1.4 mg/mL. Adenosine triphosphatase activities (3.75 and 1.97 U/mg prot) of the bacterial cells treated with allyl methyl disulfide (1.4 mg/mL) and dimethyl trisulfide (1.4 mg/mL) were distinctly lower than the activity of the control (6.05 U/mg prot). Allyl methyl disulfide (1.4 mg/mL) and dimethyl trisulfide (1.4 mg/mL) inactivated 84.20 % and 90.76 % respiratory-chain dehydrogenase of the bacterial cells, respectively. These results demonstrated that allyl methyl disulfide and dimethyl trisulfide exhibited efficient antibacterial characteristics against Escherichia coli O157:H7 and could be used as natural antibacterial agents in the prevention of Escherichia coli O157:H7 infection.

Bactericidal Mechanisms of Chlorine Dioxide against Beta-Hemolytic Streptococcus CMCC 32210

Chlorine dioxide is a globally recognized green and efficient disinfectant. This study aims to investigate the bactericidal mechanism of chlorine dioxide using beta-hemolytic Streptococcus (BHS) CMCC 32210 as a representative strain. BHS was exposed to chlorine dioxide, the minimum bactericidal concentration (MBC) values of chlorine dioxide against BHS were determined by the checkerboard method in preparation for subsequent tests. Cell morphology was observed using electron microscopy. Protein content leakage, adenosine triphosphatase (ATPase) activity, and lipid peroxidation were determined by kits, and DNA damage was determined using agar gel electrophoresis. The concentration of chlorine dioxide during disinfection showed a linear relationship with the concentration of BHS. Scanning electron microscopy (SEM) results showed that chlorine dioxide caused significant damage to the cell walls of BHS at a concentration of 50 mg/L, but had no significant effect on Streptococcus exposed to different exposure times. Furthermore, the extracellular protein concentration increased with increasing chlorine dioxide concentration, while the total protein content remained unchanged. The activities of Na+/K+-ATPase and Ca2+/Mg2+-ATPase decreased with increasing chlorine dioxide concentration. Chlorine dioxide treatment led to significant lipid peroxidation and DNA degradation in BHS. Leakage of intracellular components indicated that chlorine dioxide damaged the cell membrane of BHS. Chlorine dioxide exposure resulted in oxidative damage to lipids and proteins, which negatively impacted the cell wall and membrane of Streptococcus. This caused increased permeability and inactivation of key enzymes (Na+/K+-ATPase and Ca2+/Mg2+-ATPase) involved in respiratory metabolism, ultimately leading to DNA degradation and bacterial death due to either content leakage or metabolic failure.

The Requirement and Protective Effects of Dietary Protein against Chronic Ammonia Exposure in Juvenile Genetically Improved Farmed Tilapia (Oreochromis niloticus).

Ammonia is a key risk factor in intensive aquaculture systems. This experiment is aimed at investigating the influence of dietary protein levels on genetically improved farmed tilapia (GIFT, Oreochromis niloticus) under chronic ammonia stress. GIFT juveniles of 4.00 ± 0.55 g were exposed to high ammonia level at 0.88 mg/L and fed with six diets comprising graded protein levels at 22.64%, 27.26%, 31.04%, 35.63%, 38.47%, and 42.66% for 8 weeks. The fish in negative control was fed the diet with 31.04% protein in normal water (0.02 mg ammonia/L water). Our results showed that high ammonia exposure (0.88 mg/L) caused significant decrease in fish growth performance, hematological parameters, liver antioxidant enzymes (catalase and glutathione peroxidase), and gill Na+- and K+-dependent adenosine triphosphatase (Na+/K+-ATP) activity. When fish were under high ammonia exposure, the weight gain rate, special growth rate, feed efficiency, and survival rate elevated significantly with dietary protein supplementation increase to 35.63%, whereas protein efficiency ratio, hepatosomatic index, and viscerosomatic index showed a decreased tendency. Dietary protein administration significantly enhanced crude protein but reduced crude lipid contents in the whole fish. Fish fed diets with 35.63%-42.66% protein had higher red blood cell counts and hematocrit percentage than fish fed 22.64% protein diet. The values of serum biochemical indices (lactate dehydrogenase, aspartate aminotransferase, and alanine aminotransferase), hepatic antioxidant enzymes (superoxide dismutase, catalase, and glutathione peroxidase), and gill Na+/K+-ATP activity were all elevated with the increment of dietary protein. Moreover, histological analysis indicated that dietary protein administration could prevent the ammonia-induced damages in fish gill, kidney, and liver tissues. Based on weight gain rate as a response criterion, the optimal dietary protein requirement for GIFT juveniles under chronic ammonia stress was 37.9%.

Extract of Celosia leptostachya Leaves Inhibits Cobra Venom Toxins

Background: Celosia leptostachya belongs to Amaranthaceae plant family. Its leaves are used traditionally in the treatment of conditions, such as convulsion, eye infection and most notably to cure snakebites. This study investigated the inhibiting effect of the extract of C. leptostachya leaves against cobra snake venom in mice. Methods: We used 36 albino mice of mixed gender, weighing 20-25 g. They were divided into six groups of six rats each. Each rat was pre-treated with 0.4 mg/kg of cobra snake venom, and was subsequently given a graded dose of zero, 50, 100, 150, 200, or 250 mg/kg of the ethanol extract of C. leptostachya leaves. The animals were monitored for the survival rate. Various inhibition assays were performed to estimate the activities of acetyl cholinesterase, protease and adenosine triphosphatase of cobra venom, in the presence of 100-300 µg of the plant extract. Results: The extract inhibited the effects of cobra venom significantly after the intraperitoneal injection of the venom and extract at 20 minutes intervals. The results demonstrated that 100% of the mice survived if they received 100-250 mg/kg of the extract while only 83.3% survived with the extract at 50 mg/kg. The extract inhibited the venom’s acetyl cholinesterase, protease and adenosine triphosphatase. The inhibition occurred at higher percentages if the extract was given at 300 mg/kg. Conclusion: The plant extract significantly inhibited the snake venom, and its acetyl cholinesterase, protease and adenosine triphosphatase that mediated the venom’s toxicity.

Photo-aging promotes the inhibitory effect of polystyrene microplastics on microbial reductive dechlorination of a polychlorinated biphenyl mixture (Aroclor 1260)

Polychlorinated biphenyls (PCBs) and microplastics (MPs) commonly co-exist in various environments. MPs inevitably start aging once they enter environment. In this study, the effect of photo-aged polystyrene MPs on microbial PCB dechlorination was investigated. After a UV aging treatment, the proportion of oxygen-containing groups in MPs increased. Photo-aging promoted the inhibitory effect of MPs on microbial reductive dechlorination of PCBs, mainly attributed to the inhibition of meta-chlorine removal. The inhibitory effects on hydrogenase and adenosine triphosphatase activity by MPs increased with increasing aging degree, which may be attributed to electron transfer chain inhibition. PERMANOVA showed significant differences in microbial community structure between culturing systems with and without MPs (p < 0.05). Co-occurrence network showed a simpler structure and higher proportion of negative correlation in the presence of MPs, especially for biofilms, resulting in increased potential for competition among bacteria. MP addition altered microbial community diversity, structure, interactions, and assembly processes, which was more deterministic in biofilms than in suspension cultures, especially regarding the bins of Dehalococcoides. This study sheds light on the microbial reductive dechlorination metabolisms and mechanisms where PCBs and MPs co-exist and provides theoretical guidance for in situ application of PCB bioremediation technology.

Study of histochemical characterizations of skeletal muscle fiber types in the rabbits ( Oryctolagus Cuniculus )

This project has been conducted on New Zealand White Rabbits (newborns and adults) . Biceps brachii, soleus and abdominal wall of muscles were used in this study. Fresh pieces of muscle tissues were frozen to be cut at (10 μm) thick sections by the cryostat.Skeletal musclefibre types were investigated histochemically to demonstrate myosin adenosin triphosphatase (ATPase) activity using acid and alkaline preincubation and succinate dehydrogenase ( SDHase ) activity . In this way it may be possible to recognize the fast and slow twitch muscle fibers, as well as to explore the difference in reaching maturity between different muscles of the body. The results showed that, the biceps brachii and abdominal wall muscles consist predominantly of fast fibers, whilst the soleus muscle is made up of a near homogenous population of slow fibers. The immature abdominal wall muscle showed some reversal of the mature limb muscles staining pattern of the same animal.