Polystyrene microplastics disrupted physical barriers, microbiota composition and immune responses in the cecum of developmental Japanese quails.

Microplastics, a new type of emerging pollutant, is ubiquitous in terrestrial and water environments. Microplastics have become a growing concern due to their impacts on the environment, animal, and human health. Birds also suffer from microplastics contamination. In this study, we examined the toxic effects of polystyrene microplastics (PS-MPs) exposure on physical barrier, microbial community, and immune function in the cecum of a model bird species-Japanese quail (Coturnix japonica). The one-week-old birds were fed on environmentally relevant concentrations of 20 µg/kg, 400 µg/kg, and 8 mg/kg PS-MPs in the diet for 5 weeks. The results showed that microplastics could cause microstructural damages characterized by lamina propria damage and epithelial cell vacuolation and ultrastructural injuries including microvilli breakage and disarrangement as well as mitochondrial vacuolation in the cecum of quails. In particular, blurry tight junctions, wider desmosomes spacing, and gene expression alteration indicated cecal tight junction malfunction. Moreover, mucous layer breakdown and mucin decrease indicated that chemical barrier was disturbed by PS-MPs. PS-MPs also changed cecal microbial diversity. In addition, structural deformation of cecal tonsils and increasing proinflammatory cytokines suggested cecal immune disorder and inflammation responses by PS-MPs exposure. Our results suggested that microplastics negatively affected digestive system and might pose great health risks to terrestrial birds.

Facile, Controllable, and Ultrathin NiFe-LDH In Situ Grown on a Ni Foam by Ultrasonic Self-Etching for Highly Efficient Urine Conversion.

As the primary source of nitrogen pollutants in domestic sewage, urine is also an alternative for H2 production via electrochemical processes. However, it suffers from sluggish kinetics and noble-metal catalyst requirement. Here, we report a non-precious ultrathin NiFe-layered double hydroxide catalyst for the remarkable conversion of urea into N2 and H2, which is in situ grown on a Ni foam via ultrasonic self-etching in Fe3+/ethylene glycol (EG). EG regulates the etching rate of Fe3+, resulting in an ultrathin nanosheet structure with the aid of ultrasonication. This structure dramatically promotes the dehydrogenation process via decreasing the nanolayer thickness from 120 to 3.4 nm and leads to a 4.8-fold increase in the generation of active sites. It exhibits record urea oxidation kinetics (390.8 mA·cm-2 at 1.5 V vs RHE) with excellent stability (120 h), which is 11.8 times better than that of commercial Pt/C catalyst (33.1 mA·cm-2). Tests with real urine at 20 mA cm-2 achieve 74% total nitrogen removal and 2853 µmol·h-1 of H2 production. This study provides an attractive landscape for producing H2 by consuming urine biowastes.

Lead exposure disrupted ileal barrier of developmental Japanese quails(Coturnix japonica): Histopathological damages, microbiota dysbiosis and immune disorder.

The gut barrier plays an essential role in maintaining homeostasis and is usually composed of a mechanical barrier, a chemical barrier, an immune barrier, and a biological barrier. However, the impacts of lead (Pb) exposure on avian gut barrier are still unclear. Therefore, the present study tried to determine the toxic effects of Pb on ileal barrier of a biological model-Japanese quail (Coturnix japonica). One-week old quails were exposed to 0, 50, 500 and 1000 ppm Pb in drinking water for 5 weeks. The results showed mechanic barrier in the ileum was disrupted with microstructural deformation featured by epithelial cell abscission, villi contractions and goblet cells reduction as well as ultrastructural changes characterized by swollen mitochondria, blurry tight junctions and microvilli subtraction. Meanwhile, the expression of genes associated with intestinal tight junctions was downregulated in Pb-treated groups indicating tight junction malfunction. Moreover, less mucus and downregulation of expression of mucin2 (Muc2) and Krüppel-like factor 4 (Klf4) indicated chemical barrier disturbance by Pb. In addition, the alteration of microbial diversity and emergence of pathogen bacteria suggested ileal biological barrier disruption by Pb. Furthermore, Pb caused immune dysfunction in the ileum through promoting the expression of pro-inflammatory factors including interleukin 1 beta (IL-1ß), interleukin 6 (IL-6), Interferon gamma (IFN-γ), tumor necrosis factor alpha (TNF-α) and nuclear factor kappa B (NF-κB) and inhibiting the expression of anti-inflammatory factor interleukin 10 (IL-10). The present study demonstrated that Pb may pose health risks to birds through gut barrier damages.

Tracking the Progression of the Simulated Bronze Disease-A Laboratory X-ray Microtomography Study.

The internal three-dimensional characteristics of X-ray microtomography (micro-CT) has great application potential in the field of bronze corrosion. This work presents a method of simulating bronze disease based on an in situ micro-CT image to study the characteristics of the oxidative hydrolysis reactions of copper(I) chloride and copper(II) chloride dihydrate. A series of high-resolution reconstruction images were obtained by carrying out micro-CT at three key points throughout the experiment. We found that the reactions of copper(I) chloride and copper(II) chloride dihydrate showed different characteristics at different stages of the simulation in the micro-CT view. The method proposed in this work specifically simulated one single type of bronze corrosion and characterized the evolution characteristics of simulated bronze disease. It provides a new perspective to investigate bronze disease and can help improve the subsequent use of micro-CT to distinguish real bronze corrosions.

Transcriptomic Analysis of Hepatotoxicology of Adult Zebrafish (Danio rerio) Exposed to Environmentally Relevant Oxytetracycline.

The extensive use of the broad-spectrum antibiotics like oxytetracycline (OTC) has become a serious environmental issue globally. OTC has profound negative effects on aquatic organisms including fishes. In this study, RNA-Seq analysis was employed to examine the possible molecular mechanism of hepatotoxicology in zebrafish induced by OTC exposure. Adult male zebrafish was exposed to 0, 5, 90, and 450 µg/L OTC for 3 weeks. The results showed the decrease in body weight and tail length but the increase in total length of zebrafish under OTC exposure in a dose-dependent way. In addition, severe histopathological damages were featured by increasing tissue vacuolization in the livers of 450 µg/L OTC group. Moreover, RNA-Seq analysis revealed that molecular signaling and functional pathways in the liver were disrupted by OTC exposure. Furthermore, the down-regulation of gene expression after OTC exposure was found on both the genes related to fatty acid degradation and the genes related to lipid synthesis. The present study implied that OTC induced liver malfunction and fish health risks through growth retard, histopathological damages, molecular signaling disruption, genetic expression alteration, and lipid metabolism disturbance.

Cadmium induced skeletal underdevelopment, liver cell apoptosis and hepatic energy metabolism disorder in Bufo gargarizans larvae by disrupting thyroid hormone signaling.

Cadmium (Cd) is hazardous to human health and it is also highly detrimental to amphibian life. In this study, Bufo gargarizans larvae were exposed to environmentally relevant Cd concentrations of 5, 100 and 200 µg L-1 from Gosner stage (Gs) 26 to Gs 42 of metamorphic climax about 6 weeks. The results showed thyroid structural injuries and thyroid signaling disruption were induced by high Cd exposure (100 and 200 µg L-1). Moreover, tadpole skeleton including whole body, vertebrata, forelimb and hindlimb was developmentally delayed by high Cd exposure through downregulating the mRNA expressions of genes involved with skeletal ossification and growth pathway. Moreover, liver histopathological injuries were caused by high Cd exposure featured by hepatocytes malformation, nuclear degeneration and increasing melanomacrophage centers. Meanwhile, liver apoptosis rate showed on the rise in a dose-dependent way and Cd stimulated liver apoptosis by upregulating mRNA expressions of genes related to extrinsic and intrinsic apoptosis pathways. Furthermore, high Cd caused hepatic glucometabolism disorder by decreasing the genetic expressions associated with glycolysis and mitochondrial oxidative phosphorylation. In addition, liver lipid metabolism was disrupted by high Cd exposure through downregulating mRNA levels of genes related to fatty oxidation and upregulating mRNA levels of genes related to fatty acid synthesis. We suggested that Cd did great harm to tadpole health by disturbing thyroid function, skeletal growth, liver cell apoptosis signaling and hepatic energy metabolism pathway.

Defective Leptotene Chromosome 1 (DLC1) encodes a type-B response regulator and is required for rice meiosis.

Meiosis is critical for sexual reproduction and the generation of new allelic variations in most eukaryotes. In this study, we report the isolation of a meiotic gene, DLC1, using a map-based cloning strategy. The dlc1 mutant is sterile in both male and female gametophytes due to an earlier defect in the leptotene chromosome and subsequent abnormalities at later stages. DLC1 is strongly expressed in the pollen mother cells (PMCs) and tapetum and encodes a nucleus-located rice type-B response regulator (RR) with transcriptional activity. Further investigations showed that DLC1 interacts with all five putative rice histidine phosphotransfer proteins (HPs) in yeast and planta cells, suggesting a possible participation of the two-component signalling systems (TCS) in rice meiosis. Our results demonstrated that DLC1 is required for rice meiosis and fertility, providing useful information for the role of TCS in rice meiosis.

The effects of chronic lead exposure on the ovaries of female juvenile Japanese quails (Coturnix japonica): Developmental delay, histopathological alterations, hormone release disruption and gene expression disorder.

Lead (Pb) is well-recognized for its great hazards to human and wildlife health. It has negative influences on multiple organs and systems of birds. Especially, lead exposure caused adverse impacts on bird reproduction. In this study, one week old female Japanese quails were randomly allocated into four groups and each group was respectively fed with 0, 50 ppm, 500 ppm and 1000 ppm Pb in drinking water for 36 days to determine the effects of chronic lead exposure on ovarian development and function. The results showed that Pb did accumulate in the ovary and ovarian development was delayed by high dose lead exposure (500 ppm and 1000 ppm). Moreover, high Pb dosage induced ovarian histopathological damages characterized by granulosa cells disorganization, follicle atresia and interstitial cell degeneration. Meanwhile, the concentration of estradiol (E2) was significantly decreased and mRNA levels of genes involved with ovarian steroidogenesis were significantly down-regulated by high concentration Pb. In addition, Pb exposure caused increasing cell apoptosis and significant changes of the expression of genes involved with cell death in the ovary. High dose Pb exposure also inhibited thyroid hormone release and disrupted ovarian thyroid deiodination apart from causing thyroid histopathological injury such as follicular deformation and atrophy. The study indicated that Pb might cause ovarian malfunction by inducing ovary and thyroid microstructural damages, thyroid hormone and estrogen release inhibition and ovarian steroidogenesis disruption.

The effects of chronic cadmium exposure on the gut of Bufo gargarizans larvae at metamorphic climax: Histopathological impairments, microbiota changes and intestinal remodeling disruption.

Cadmium (Cd) is carcinogenic to human and it also has adverse effects on aquatic life such as amphibian larvae. However, its influences on amphibian gut morphology and development as well as intestinal microbiota are still hardly understood. In this study, we examined the effects of chronic cadmium exposure on the gut of tadpoles at Gosner stage 42 of metamorphic climax by using Bufo gargarizans as a model species. Tadpoles were exposed to cadmium concentrations at 0, 5, 100 and 200 µg L-1 from Gosner stage 26-42. The results showed that high cadmium (100 and 200 µg L-1) exposure caused significant decrease of body length and weight but significant increase of intestinal length and weight. Moreover, severe histopathological damages were induced by high Cd exposure. In addition, microbial communities in the gut of tadpoles in high cadmium exposure groups were remarkably different from those in control group. Unexpectedly, species diversity and richness were higher in the intestinal microbiota of 200 µg L-1 cadmium exposure group. Furthermore, the abundance of prevalent phyla, families and genera of intestinal microbiota were changed by cadmium exposure. Meanwhile, cadmium exposure perturbed gut renewal functions and the relative mRNA expression of genes involved in canonical and non-canonical Wnt signaling pathway was seriously affected by high cadmium exposure. We concluded that cadmium could be harmful to tadpole health by inducing intestinal histopathological damages, gut remodeling inhibition and intestinal microbiota alterations.

The effects of chronic lead exposure on the liver of female Japanese quail (Coturnix japonica): Histopathological damages, oxidative stress and AMP-activated protein kinase based lipid metabolism disorder.

Lead (Pb) is one of the most toxic metals to human and wildlife. It also had multiple negative influences on birds with physical, neurological and hematological clinical signs. However, the impacts of lead on bird liver lipid metabolism are still unclear. In this study, female Japanese quails were used to examine the effects of chronic lead exposure on liver histology, oxidative stress and AMPK (AMP-activated protein kinase) based lipid metabolism. Quails were randomly divided into 5 groups and each group was respectively fed with 0, 50, 250, 500 and 1000 ppm lead solution for 49 days. The result showed that exposure to 250, 500 and 1000 ppm Pb induced severe histopathological damages characterized by liver lipid vacuoles and accumulation, hepatic cytoplasmic hyalinization and vacuolization, hepatocytes necrosis, hepatic sinusoid congestion, and it also caused ultrastructural alterations featured by swelling and vacuolar mitochondria, the depolymerization of polyribosome, and lipid droplets accumulation. Moreover, significant decrease of activities of GPx (glutathione peroxidase), SOD (superoxide dismutase), CAT (catalase) and level of T-AOC (total antioxidant capacity) while significant increase of MDA (malondialdehyde) content were found in livers of all Pb groups. In addition, the expressions of genes related to fatty synthesis were significantly upregulated in livers of all Pb groups while the expressions of genes related to fatty ß-oxidation were significantly downregulated in livers of 250 ppm Pb group. The present study indicated lead exposure does cause bird health damages through inducing liver microstructural and ultrastructural injury, oxidative damages and lipid metabolism disorder.

Exposure to cadmium induced gut histopathological damages and microbiota alterations of Chinese toad (Bufo gargarizans) larvae.

Cadmium (Cd) is highly hazardous to both terrestrial and aquatic life and it also has multiple negative impacts on amphibian tadpoles and frogs. However, its effects on gut health of amphibian tadpoles are still poorly understood. We used Chinese toad (Bufo gargarizans) tadpoles to examine the effects of chronic cadmium exposure on gut histology and intestinal microbiota by using regular histology analysis and high-throughput sequencing techniques. Tadpoles were exposed to cadmium concentrations at 0, 5, 100 and 200 µg L-1 from Gosner stage 26 to 38. Our results showed 100 and 200 µg L-1 cadmium exposure caused severe gut histopathological alterations while 5 µg L-1 cadmium exposure induced subtle intestine damage. Moreover, species diversity, taxonomic composition and community structure of gut microbiota were influenced by cadmium exposure. Species diversity and richness decreased gradually with the increase of cadmium concentration. Microbial communities of tadpoles in 100 and 200 µg L-1 cadmium exposure groups were remarkably different from those in control group. Furthermore, the relative abundances of prevalent phyla such as Proteobacteria, Bacteroidetes and Firmicutes and dominant genera such as Klebsiella and Aeromonas were also affected by cadmium exposure. We concluded that cadmium could be harmful to tadpole health by inducing intestinal damages and gut microbiota changes.

Chronic lead exposure induces histopathological damage, microbiota dysbiosis and immune disorder in the cecum of female Japanese quails (Coturnix japonica).

Lead (Pb) is one of the most hazardous metals to human and wildlife and it also has multiple negative impacts on birds. However, its influences on bird gut morphology and intestinal microbiota were still unclear. We used female Japanese quails (Coturnix japonica) to examine the effects of chronic lead exposure (0, 50 ppm and 1000 ppm) on cecal histology, microbial communities and immune function. The results showed 50 ppm lead exposure caused subtle damages of cecum cell structure. However, 1000 ppm lead exposure caused severe cecum histopathological changes characterized by mucosa abscission, Lieberkühn glands destruction and lymphocyte proliferation. Moreover, both lead concentrations induced ultrastructural damages featured by nucleus pyknosis, mitochondrial vacuolation and microvilli contraction. Meanwhile, microbial community structure, species diversity, taxonomic compositions and taxa abundance in the cecum were affected by lead exposure. Furthermore, the mRNA relative expression of immunity-related genes such as interleukin 2 (IL-2) and gamma interferon (IFN-γ) was significantly downregulated while that of interleukin 6 (IL-6), tumor necrosis factor α (TNF-α) and natural killer kappa B (NF-κB) was significantly upregulated in the cecum of 50 and 1000 ppm lead exposure groups. We concluded that lead exposure may cause gut health impairment of female Japanese quails by inducing cecal histopathological changes, microbiota dysbiosis and cecal immune disorder.

Chronic effects of mercury on Bufo gargarizans larvae: Thyroid disruption, liver damage, oxidative stress and lipid metabolism disorder.

Mercury is severely detrimental to organisms and is ubiquitous in both terrestrial and aquatic ecosystems. In the present study, we examined the effects of chronic mercury (Hg) exposure on metamorphosis, body size, thyroid microstructures, liver microstructural and ultrastructural features, and transcript levels of genes associated with lipid metabolism, oxidative stress and thyroid hormones signaling pathways of Chinese toad (Bufo gargarizans) tadpoles. Tadpoles were exposed to mercury concentrations at 0, 6, 12, 18, 24 and 30 µg/L from Gosner stage 26-42 of metamorphic climax. The present results showed that high dose mercury (24 and 30 µg/L) decelerated metamorphosis rate and inhibited body size of B. gargarizans larvae. Histological examinations have clearly exhibited that high mercury concentrations caused thyroid gland and liver damages. Moreover, degeneration and disintegration of hepatocytes, mitochondrial vacuolation, and endoplasmic reticulum breakdown were visible in the ultrastructure of liver after high dose mercury treatment. Furthermore, the larvae exposed to high dose mercury demonstrated a significant decrease in type II iodothyronine deiodinase (Dio2) and thyroid hormone receptor α and ß (TRα and TRß) mRNA levels. Transcript level of superoxide dismutase (SOD) and heat shock protein (HSP) were significantly up regulated in larvae exposed to high dose mercury, while transcript level of phospholipid hydroperoxide glutathione peroxidase (PHGPx) was significantly down regulated. Moreover, exposure to high dose mercury significantly down regulated mRNA expression of carnitine palmitoyltransferase (CPT), sterol carrier protein (SCP), acyl-CoA oxidase (ACOX) and peroxisome proliferator-activated receptor α (PPAPα), but significantly up regulated mRNA expression of fatty acid elongase (FAE), fatty acid synthetase (FAS) and Acetyl CoA Carboxylase (ACC). Therefore, we conclude that high dose mercury induced thyroid function disruption, liver oxidative stress and lipid metabolism disorder by damaging thyroid and liver cell structures and altering the expression levels of relevant genes.

Chronic Effects of Fluoride Exposure on Growth, Metamorphosis, and Skeleton Development in Bufo gargarizans Larvae.

Bufo gargarizans tadpoles were chronically exposed to waterborne fluoride at measured concentrations ranging from 0.4 to 61.2 mg F-/L for 70 days from Gosner stage 26 to completion of metamorphosis. The chronic exposure caused a concentration-dependent mortality in all tested fluoride concentrations. Total length, snout-to-vent length (SVL), body mass, and developmental stage of tadpoles were significantly inhibited at 42.6 mg F-/L. In addition, significant metamorphic delay and increase in size at completion of metamorphosis occurred after exposure to 19.8 mg F-/L. Moreover, 19.8 mg F-/L suppressed the bone mineralization of larvae at completion of metamorphosis. However, the bone mineralization could be enhanced by 4.1 mg F-/L. In conclusion, our results suggested that the presence of high concentrations of fluoride could increase mortality risk, delay metamorphosis, and suppress skeletal ossification in B. gargarizans larvae.

Effects of fluoride on development and growth of Rana chensinensis embryos and larvae.

The present study examined the adverse effects of fluoride exposure on embryos and larvae of Rana chensinensis. Survival, morphological abnormalities, growth and development, time to metamorphosis and size at metamorphic climax of R. chensinensis were examined. Our results showed that embryos malformation occurred in all fluoride treatments. Morphological abnormalities of embryos are characterized by axial flexures, the extrusion of fin axis, edema, and ruffled dorsal and ventral fin. Additionally, 4.1mg F(-)/L and above could significantly inhibit embryos growth and development. On day 15, total length and weight of tadpole were significantly lower in 19.6 and 42.4 mg F(-)/L treatments compared to control. However, significant reductions in total length and weight were observed only at 42.4 mg F(-)/L on day 30. Moreover, significant metamorphic delay and decrease in the size at metamorphic climax were found in larvae exposed to 42.4 mg F(-)/L. Taken together, embryos of R. chensinensis are more vulnerable to fluoride exposure than their tadpoles. Our results suggested that the presence of high concentrations fluoride might increase mortality risk and a reduction in juvenile recruitment in the field by increasing embryos malformation, delaying metamorphosis and decreasing size at metamorphosis.

Chronic effects of triclosan on embryonic development of Chinese toad, Bufo gargarizans.

Triclosan (TCS) is commonly used worldwide in a range of personal care and sanitizing products. The aim of this study was to evaluate potential effects of TCS exposure on embryonic development of Bufo gargarizans, an endemic frog species in China. Standard Gosner stage 3 B. gargarizans embryos were exposed to 10 ~ 150 µg/L TCS during embryogenesis. Survival, total length, weight, developmental stage, duration of different embryo stages, malformation, and type II and III deiodinase (D2 and D3) expression were measured. Inhibitory effects on embryo developmental stage, total length and weight were found at 30 ~ 150 µg/L TCS. Moreover, the duration of embryonic development was increased at gastrula, neural, circulation, and operculum development stage in TCS-treated groups. In addition, TCS exposure induced morphological malformations in B. gargarizans embryos, which are characterized by hyperplasia, abdominal edema, and axial flexures. Furthermore, our results showed that the expression of D2 in embryos was probably down-regulated at 60 and 150 µg/L TCS, but its spatial expression patterns was not affected by TCS. In summary, our study suggested that TCS exposure not only resulted in delayed growth and development but also caused teratogenic effects in B. gargarizans embryos, and the developmental effects of TCS at high concentrations may be associated with disruption of THs homeostasis. Although further studies are necessary, the present findings could provide a basis for understanding on harmful effects and the potential mechanisms of TCS in amphibian embryos.

Breeding habitat survey of blackthroat (Luscinia obscura) in Foping nature reserve of Qinling Mountains.

We carried out a primary survey by quadrat sampling to quantify breeding habitat characteristics of blackthroat (Luscnia obscura), a poorly documented and vulnerable bird species, in Foping nature reserve on the central southern Qinling Mountains. Tree layer information was collected in 10 m × 10 m plots, bamboo and shrub layer information was collected in 2 m × 2 m plots, and grass and ground layer information was collected in 1 m × 1 m plots. Our observations showed that blackthroat lives in coniferous forest and coniferous broadleaved forest with dense bamboos at the elevation ranging from 2130 m to 2600 m. Shrub cover, density and height, and ground cover in sites with blackthroat were significantly higher than those in random sites, while tree density, grass height and cover in habitat sites were significantly lower than those in random sites. These results suggest that shrub cover, shrub density, and canopy cover may be relevant to breeding habitat selection by these birds. Our study suggests that Qinling Mountains may be an important blackthroat breeding site.

Microplastics induced inflammation in the spleen of developmental Japanese quail (Coturnix japonica) via ROS-mediated p38 MAPK and TNF signaling pathway activation1.

Microplastics (MPs) have been found in virtually every environment on earth and become a source of pollution around the world. The toxicology of microplastics on immunity is an emerging area of research, and more studies are needed to fully understand the effects of microplastics exposure on animal health. Therefore, we tried to determine the immunotoxic effects of microplastics on avian spleen by using an animal model- Japanese quail (Coturnix japonica). One-week chicks were exposed to environmentally relevant concentrations of 0.02 mg/kg, 0.4 mg/kg and 8 mg/kg polystyrene microplastics in the feed for 5 weeks. The results demonstrated that microplastics induced microstructural injuries featured by cell disarrangement and vacuolation indicating splenic inflammation. Ultrastructural damages including membrane lysis and mitochondrial vacuolation also suggested inflammatory responses in the spleen by microplastics exposure. Meanwhile, increasing reactive oxygen species (ROS) and Malondialdehyde (MDA) while the inactivation of superoxide dismutase (SOD), catalase (CAT) and glutathione S-transferase (GST) indicated oxidative stress in the spleen. Moreover, the increasing level of proinflammatory cytokines including Tumor necrosis factor alpha (TNF-α), interferon gamma (IFN-γ), interleukin-1ß (IL-1ß), interleukin-6 (IL-6) and decreasing level of anti-inflammatory cytokine interleukin-10 (IL-10) implied splenic inflammation. Furthermore, transcriptomic analysis showed that microplastics induced inflammatory responses in the spleen through p38 mitogen-activated protein kinases (p38 MAPK) pathway activation and tumor necrosis factor (TNF) signaling stimulation. The signaling stimulation also aggravated cell apoptosis in the spleen. The present study may benefit to understand potential mechanisms of developmental immunotoxicology of microplastics.

Lead induced cerebellar toxicology of developmental Japanese quail (Coturnix japonica) via oxidative stress-based Nrf2/Keap1 pathway inhibition and glutathione-mediated apoptosis signaling activation.

Lead (Pb) is a heavy metal that has been recognized as a neurotoxin, meaning it can cause harmful effects on the nervous system. However, the neurotoxicology of Pb to birds still needs further study. In this study, we examined the neurotoxic effects of Pb exposure on avian cerebellum by using an animal model-Japanese quail (Coturnix japonica). The one-week old male chicks were exposed to 50, 200 and 500 mg/kg Pb of environmental relevance in the feed for five weeks. The results showed Pb caused cerebellar microstructural damages charactered by deformation of neuroglia cells, granule cells and Purkinje cells with Nissl body changes. Moreover, cerebellar neurotransmission was disturbed by Pb with increasing acetylcholine (ACh) and decreasing acetylcholinesterase (AChE), dopamine (DA), γ-Aminobutyric Acid (GABA) and Na+/K+ ATPase. Meanwhile, cerebellar oxidative stress was caused by Pb exposure represented by increasing reactive oxygen species (ROS) and malondialdehyde (MDA) as well as decreasing catalase (CAT), glutathione peroxidase (GPX), glutathione (GSH) and superoxide dismutase (SOD). Moreover, RNA-Seq analysis showed that molecular signaling pathways in the cerebellum were disrupted by Pb exposure. In particular, the disruption of nuclear factor erythroid-2-related factor 2 (Nfr2)/kelch-like ECH-associated protein 1 (Keap1) pathway and glutathione metabolism pathway indicated increasing cell apoptosis and functional disorder in the cerebellum. The present study revealed that Pb induced cerebellar toxicology through structural injury, oxidative stress, neurotransmission interference and abnormal apoptosis.

From pill to pain: Alendronate-induced esophageal injury-A case report and review.

Background: Alendronate is used to treat Paget's bone disease, glucocorticoid-induced osteoporosis, and postmenopausal osteoporosis because it suppresses osteoclast activity to stop bone resorption. Case report: We present an exceptional case of esophagitis caused by alendronate. Blood tests and other data were normal when the patient was taken to the hospital, but an endoscopic examination revealed significant esophageal redness, erosion, and ulceration, along with pseudomembrane. The patient was given medicine after receiving a diagnosis of alendronate pill-induced esophagitis based on the pathological findings. Conclusion: This case report is a timely reminder of the importance of thorough pharmacovigilance, patient education, and smart therapeutic decision-making in the context of alendronate use. To properly treat and prevent problems with the esophagus caused by alendronate, additional research is required.