Acute Exposure Group Research Articles

Study on low concentration deltamethrin toxicity mediated by phospholipase D in Chinese mitten crab (Eriocheir sinensis) ovary

This study evaluates the impact of environmentally relevant, low-concentration deltamethrin exposure to Eriocheir sinensis ovaries. Our findings revealed that even at a concentration of 0.05 µg/L, deltamethrin exposure can induce significant ovarian toxicity through a 5-day exposure, with gradual amplification detected with time, demonstrating the toxicity amplification effect. Hematoxylin and Eosin staining revealed that low-concentration deltamethrin exposure produces pathological damage consistent with acute toxicity—yolk granules were dissolved and oocyte membranes were ruptured. High-throughput RNA-sequencing data indicated that the acute and low-concentration exposure groups involved completely different pathways and molecular functions, suggesting distinct mechanisms for their toxic effects. Following the identification of phospholipase D (PLD) as a potential core factor regulating the toxicity amplification effect of low concentration deltamethrin, we delved into subsequent mechanism studies using quantitative real-time PCR, immunofluorescence and enzyme-linked immunosorbent assay. Through the GnRH signaling pathway, increased PLD indirectly stimulates augmented estradiol secretion, subsequently inducing apoptosis by upregulating Cathepsin D, which can activate the key executioners of apoptosis—caspases (CASP3 and CASP7). In conclusion, low-concentration deltamethrin exposures can induce significant ovarian damage through apoptosis mediated by the upregulation of PLD in the ovaries of Eriocheir sinensis at environmentally relevant concentrations, which lays the preliminary theoretical groundwork for further elucidating the mechanism of toxicity amplification effect of pesticide exposure at low concentrations.

Beta-Cyfluthrin-Induced Hepatic Alterations in Zebrafish: Enzymatic Profiles and Oxidative Stress Responses

Beta-Cyfluthrin is a widely used pesticide belonging to class of synthetic pyrethroids which affects the central and peripheral nervous systems. The current study investigates the impact of beta-Cyfluthrin on the biochemical parameters of liver of zebrafish (Danio sp.). Adult zebrafish were exposed to concentrations of 0.25, 0.5, 1.0, 2.0 and 4.0 µg/L of beta-Cyfluthrin for acute (96 hours) and chronic (21 days) exposure periods respectively (n=20). It was observed that exposure to beta-Cyfluthrin led to variations in biochemical markers in both acute and chronic exposure groups. Liver function tests revealed significant elevated activity of alanine transaminase (ALT) and aspartate transaminase (AST) at exposure concentrations of 2.0 and 4.0 µg/L of beta-Cyfluthrin in both acute and chronic groups, while acid phosphatase (ACP) and alkaline phosphatase (ALP) activity decreased significantly at concentrations of 1.0, 2.0 and 4.0 µg/L in the chronic group. Lipid peroxidation exhibited a concentration and time-dependent increase with significant difference at 1.0, 2.0 and 4.0 µg/L in both acute and chronic groups, while superoxide dismutase (SOD) and peroxidase (PER) levels declined significantly in both acute and chronic exposure groups at exposure concentrations of 1.0, 2.0 and 4.0 µg/L for SOD and 2.0 and 4.0 µg/L for PER. Catalase (CAT) initially increased significantly in acute groups of 1.0, 2.0 and 4.0 µg/L but decreased in chronic ones. Glutathione S-transferase (GST) levels exhibited a significant increase at lower concentrations of 0.25 µg/L but a decrease at higher concentrations, 1.0, 2.0 and 4.0 µg/L of beta-Cyfluthrin. The level of significance were considered at p<0.05 and p<0.01. This research suggests that exposure to beta-Cyfluthrin leads to hepatic damage in adult zebrafish. This indicates a potential risk to non-target aquatic fauna, through runoff where beta-Cyfluthrin is used as an agricultural pesticide.

Validation of the Athens Insomnia Scale Among Young Chinese Male Population in a High-Altitude Situation.

The Athens Insomnia Scale (AIS) is a widely used and authorized questionnaire for evaluating insomnia symptoms. However, its reliability and validity at high altitudes are uncertain. Therefore, this study aimed to confirm the validity and reliability of AIS during a 3658 m altitude exposure. A total of 387 young Chinese males were enlisted in the acute high-altitude exposure group. They flew for about two hours, climbing from 400 m to 3658 m. The high-altitude-acclimated group consisted of 86 young Chinese men who had lived at least six months at 3658 m altitude. The sleep quality of the acute high-altitude exposure group was evaluated using the AIS before the ascent and after exposure to 3658 m for 24 hours, and one week. The sleep quality of the high-altitude-acclimated group was also assessed. The AIS's internal consistency, reliability, and validity were evaluated. The respondents' quality of sleep significantly decreased after being exposed to 3658 m as opposed to 400 m. Two factors comprised the AIS, according to an exploratory factor analysis: "sleep problem" (items 1-5) and "daytime dysfunction" (items 6-8). The Cronbach's α internal consistency coefficients exceeded 0.8, and the corrected item-total correlations were all greater than 0.5 when the subjects were exposed to 3658 m. The model fit index was well within the criterion. The average variance extracted and composite reliability were all higher than 0.5 and 0.7, respectively. The interclass correlation coefficient was deemed "fair to good" at 0.482, which is greater than the 0.4 threshold. The AIS has satisfactory discriminant validity, as shown by the Fornell-Larcker criterion and cross-loading results. The daytime dysfunction R-square values (>0.33) show that the frameworks have considerable predictive accuracy. The AIS exhibits strong consistency, reliability, and validity. The AIS's features and simplicity make it an essential psychometric tool for high-altitude sleep research.

A study on the possible neurotoxic effects of CUMYL-4CN-BINACA in Sprague Dawley rats

Substances such as Δ9-tetrahydrocannabinol (THC) and cannabidiol cross the blood–brain barrier. Detecting the damage of these substances in the brain provides important data in drug abuse studies. The aim of the study is to define the neurotoxicity of a novel synthetic cannabinoid (CUMYL-4CN-BINACA) in the Sprague-Dawley rats. Histopathological, immunohistochemical, behavioral, and biochemical examinations were performed to determine the acute and subacute toxicity of the cannabinoid. Three cannabinoid doses were administered for 2 days in the acute exposure groups and 14 days in the subacute exposure groups. Observations were made for 14 days and various changes such as mortality, injury, and illness were recorded daily. No mortality was determined. Serious pathological changes such as neurodegeneration, focal plague formation, vacuolation, edema, congestion, and fibrosis were observed in the cerebral cortex and hippocampus of the brain in a dose-dependent manner. Brain tissue caspase-3 activity showed that the cannabinoid triggered apoptosis in the rat brain. The detected cellular oxidative stress (higher lipid peroxidation and lower antioxidant enzyme activity) also supported neurotoxicity. Significant behavioral abnormalities were also observed in the acute groups, while no behavioral changes were detected in the subacute groups. This study showed for the first time that CUMYL-4CN-BINACA adversely affects the rat brain. It can be estimated that the abuse of the cannabinoid may harm human health in the same way.

Metabolic variation and oxidative stress response of blue mussels (Mytilus sp.) perturbed by norfloxacin exposure.

Antibiotics are currently widely applied in agricultural cultivation, animal husbandry, and medical treatment, but the effects and ecological risks of antibiotics need to be further investigated. Norfloxacin is one of the most widely applied fluoroquinolone antibiotics and is commonly detected in aquatic ecosystems. In this study, the activities of catalase (CAT) and glutathione S-transferase (GST) in blue mussels (Mytilus sp.) exposed to norfloxacin (from 25 to 200mg/L) for 2 d of acute exposure and 7 d of subacute exposure were measured. 1H nuclear magnetic resonance (1H-NMR)-based metabolomics was applied to identify the metabolites and to investigate the physiological metabolism of blue mussels (Mytilus sp.) under different concentrations of norfloxacin. The activity of the CAT enzyme was induced in acute exposure, while the activity of GST was inhibited in subacute exposure when the concentration of norfloxacin reached 200mg/L. Orthogonal partial least squares discriminant analysis (OPLS-DA) revealed that the increased concentrations of norfloxacin might cause greater metabolic differences between the treatment and control groups and cause greater metabolic variation within the same treatment group. The contents of taurine in the 150mg/L acute exposure group were 5.17 times higher than those in the control group. The pathway analysis indicated that exposure to high concentrations of norfloxacin disturbed different pathways involved in energy metabolism, amino acid metabolism, neuroregulation, and the regulation of osmotic pressure. These results may provide a molecular and metabolic view of the effects of norfloxacin and the regulatory mechanism of blue mussels when exposed to extremely high doses of antibiotics.

Physiological and transcriptomic effects of hexafluoropropylene oxide dimer acid in Caenorhabditis elegans during development.

Per- and polyfluoroalkyl substances (PFAS) are chemicals resistant to degradation. While such a feature is desirable in consumer and industrial products, some PFAS, including perfluorooctanoic acid (PFOA), are toxic and bioaccumulate. Hexafluoropropylene oxide dimer acid (HFPO-DA), an emerging PFAS developed to replace PFOA, has not been extensively studied. To evaluate the potential toxicity of HFPO-DA with a cost- and time-efficient approach, we exposed C. elegans larvae for 48h to 4×10-9-4g/L HFPO-DA in liquid media and measured developmental, behavioral, locomotor, and transcriptional effects at various exposure levels. Worms exposed to 1.5-4g/L HFPO-DA were developmentally delayed, and progeny production was significantly delayed (p<0.05) in worms exposed to 2-4g/L HFPO-DA. Statistically significant differential gene expression was identified in all fourteen HFPO-DA exposure groups ranging from 1.25×10-5 to 4g/L, except for 6.25×10-5 g/L. Among 10298 analyzed genes, 2624 differentially expressed genes (DEGs) were identified in the developmentally delayed 4g/L group only, and 78 genes were differentially expressed in at least one of the thirteen groups testing 1.25×10-5-2g/L HFPO-DA exposures. Genes encoding for detoxification enzymes including cytochrome P450 and UDP glucuronosyltransferases were upregulated in 0.25-4g/L acute exposure groups. DEGs were also identified in lower exposure level groups, though they did not share biological functions except for six ribosomal protein-coding genes. While our transcriptional data is inconclusive to infer mechanisms of toxicity, the significant gene expression differences at 1.25×10-5 g/L, the lowest concentration tested for transcriptional changes, calls for further targeted analyses of low-dose HFPO-DA exposure effects.

Neuroligin-1 plays an important role in methamphetamine-induced hippocampal synaptic plasticity

The neurotoxic effects of methamphetamine (METH) include not only neuronal apoptosis and autophagy, but also lead to substance use disorder and have become increasingly prominent. Studies suggest that synaptic plasticity may be the structural basis of METH-induced neurological impairment. Neuroligins are postsynaptic adhesion molecules involved in the regulation of synaptic organization and function. Animal studies have shown that neuroligin (NLG)− 1 is involved in memory formation; however, its role in METH-induced neurotoxicity is not clear. In the present study, we used 1 mM METH in vitro; mice in the acute and subacute exposure groups received intraperitoneal injections of 30 mg/kg METH (1 injection) or 15 mg/kg METH (8 separate injections at 12-h intervals). We found that the expression of NLG-1, Synapsin-1, and postsynaptic density-95 were increased after METH exposure. We further observed that METH-induced inhibition of long-term potentiation and spatial memory loss could be alleviated when mice were pretreated with NLG-1 small interfering RNA. Therefore, our study provides evidence that NLG-1 is involved in METH-induced hippocampal synaptic plasticity and may be a potential target for the treatment of METH-induced neurotoxicity.

Insights into the response mechanism of Litopenaeus vannamei exposed to cold stress during live transport combining untargeted metabolomics and biochemical assays

Unfavorable conditions severely affect the survival quality of Litopenaeus vannamei (L. vannamei) during live transport and the molecular response mechanism needs to be clarified. In this study, metabolomics combined with conventional assay on physiological and histopathological responses were applied to deepen the understanding of L. vannamei to cold stress and provide. A solid foundation for regulation of transportation management. Physiological and biochemical analysis revealed the significant disturbance of glycolysis in hepatopancreas tissue. Furthermore, metabolomics based on the technique of ultra-performance liquid chromatography quadrupole time-of-flight mass spectrometry identified the significantly differential metabolites between acute cold exposure (AC) and normal control (NC) groups. Moreover, KEEG result indicated that the pathways of amino acid, glycerophospholipid, and nuclei acid metabolism and ABC transporters in hepatopancreas were significantly disturbed. Furthermore, histopathology and ultrastructure verified the impairment in hepatopancreas during cold stress. Overall, the concurrent use of metabolomics and biochemical assays was demonstrated to be sensitive and effective in providing new insights into the response mechanism of L. vannamei to cold stress.

Hibernation with rhythmicity: the circadian clock and hormonal adaptations of the hibernating Asiatic toads (Bufo gargarizans).

Hibernation is one of the fundamental strategies in response to cold environmental temperatures. During hibernation, the endocrine and circadian systems ensure minimal expenditure of energy for survival. The circadian rhythms of key hormones, melatonin (MT), corticosterone (CORT), triiodothyronine (T3 ), and thyroxine (T4 ), and the underlying molecular regulatory mechanisms of hibernation have been well determined in mammals but not in ectotherms. Here, a terrestrial hibernating species, Asiatic toad (Bufo gargarizans), was employed to investigate the plasma CORT, MT, T3 , and T4 ; and the retina, brain, and liver mRNA expression of the core clock genes, including circadian locomotor output cycles kaput (Clock), brain and muscle ARNT-like 1 (Bmal1), cryptochrome (Cry) 1 and 2, and period (Per) 1 and 2, at 7-time points over a 24-h period under acute cold (1 day at 4°C), and hibernation (45 days at 4°C). Our results showed that the circadian rhythms of the core clock genes were rather unaffected by acute cold exposure in the retina, unlike the brain and liver. In contrast, during hibernation, the liver clock genes displayed significant circadian oscillations, while those in the retina and brain stopped ticking. Furthermore, plasma CORT expressed circadian oscillations in both groups, and T3 in acute cold exposure group, whereas T4 and MT did not. Our results reveal that the plasma CORT and the liver sustain rhythmicity when the brain was not, indicating that the liver clock along with the adrenal clock synergistically maintains the metabolic requirements to ensure basic survival in hibernating Asiatic toads.

Differential organization of open field behavior in mice following acute or chronic simulated GCR exposure

Astronauts undertaking deep space travel will receive chronic exposure to the mixed spectrum of particles that comprise Galactic Cosmic Radiation (GCR). Exposure to the different charged particles of varied fluence and energy that characterize GCR may impact neural systems that support performance on mission critical tasks. Indeed, growing evidence derived from years of terrestrial-based simulations of the space radiation environment using rodents has indicated that a variety of exposure scenarios can result in significant and long-lasting decrements to CNS functionality. Many of the behavioral tasks used to quantify radiation effects on the CNS depend on neural systems that support maintaining spatial orientation and organization of rodent open field behavior. The current study examined the effects of acute or chronic exposure to simulated GCR on the organization of open field behavior under conditions with varied access to environmental cues in male and female C57BL/6 J mice. In general, groups exhibited similar organization of open field behavior under dark and light conditions. Two exceptions were noted: the acute exposure group exhibited significantly slower and more circuitous homeward progressions relative to the chronic group under light conditions. These results demonstrate the potential of open field behavior organization to discriminate between the effects of select GCR exposure paradigms.

367 Placental histology of acute versus chronic meconium exposure- association with obstetric and neonatal outcomes

We aimed to compare obstetric and neonatal outcomes of deliveries complicated by meconium stained amniotic fluid (MSAF), according to placental histology of chronic vs. acute meconium associated changes. This was a retrospective cohort study of singleton deliveries complicated by MSAF at a single university-affiliated medical center during 2008-2018. Obstetric and neonatal outcomes were compared between cases with placental chronic vs. acute meconium exposure associated changes. Regression analysis was used to identify independent associations with adverse neonatal outcomes. The medical records of 294 deliveries at our institution were reviewed, along with medical records of the neonates and the histopathological reports of their placentas. Ninety-two cases were classified as an acute placental reaction to meconium (acute exposure group) and 200 as chronic placental exposure (chronic exposure group). Patient demographics did not differ between groups. Placentas from the chronic exposure to meconium were associated with a higher rate of placental weight <10th percentile (p=0.03) while the acute exposure group was associated with a shorter time between rupture of membranes and delivery (p=0.02) and a higher rate of adverse neonatal outcomes (p=0.02). In multivariable analysis adverse neonatal outcome was associated with acute histologic exposure to meconium independent of background confounders (aOR=1.51, 95% CI 1.12 - 3.67). Acute histological changes of MSAF were independently associated with adverse neonatal outcomes as compared to chronic histologic MSAF.View Large Image Figure ViewerDownload Hi-res image Download (PPT)

Placental histology of acute versus continuous meconium exposure - Association with obstetric and neonatal outcomes

ObjectiveWe aimed to compare obstetric and neonatal outcomes of deliveries complicated by meconium stained amniotic fluid (MSAF), according to placental histology of continuous vs. acute meconium associated changes. MethodsThis was a retrospective cohort study of singleton deliveries complicated by MSAF at a single university-affiliated medical center during 2008–2018. Obstetric and neonatal outcomes were compared between cases with placental acute vs. continuous meconium exposure associated changes (columnar epithelial changes and meconium-laden macrophages, respectively). Regression analysis was used to identify independent associations with adverse neonatal outcomes. ResultsThe medical records of 294 deliveries at our institution were reviewed, along with medical records of the neonates and the histopathological reports of their placentas. Ninety-two cases were classified as an acute placental reaction to meconium (acute exposure group) and 200 as continuous placental exposure (continuous exposure group). Patient demographics did not differ between groups. Placentas from the continuous exposure to meconium were associated with a higher rate of placental weight <10th percentile (p = 0.03) while the acute exposure group was associated with a shorter time between rupture of membranes and delivery (p = 0.02). and higher rates of non-reassuring fetal heart rate in labor (p = 0.003), and of adverse neonatal outcome (p = 0.02). In multivariable analysis adverse neonatal outcome was associated with acute histologic exposure to meconium independent of background confounders (aOR = 1.51, 95% CI 1.12–3.67). ConclusionsAcute histological changes of MSAF were independently associated with adverse neonatal outcomes as compared to continuous histologic MSAF.

Effect of Oral Administration of Ibuprofen on Prothrombin Time, Activated Partial Thromboplastin and Platelet Count in Wistar Albino Rats

Aim: Ibuprofen is analgesic, antipyretic and anti-inflammatory drug, which is widely used as a cheap over- the counter drug (OTC); however, this drug accompanies anti coagulation/anti platelets effects which sometimes might illicit adverse effects. In this study, we investigated effect of ibuprofen on prothrombin time (PT), activated partial thromboplastin time (aPTT) and platelet count using wistar albino rats.&#x0D; Methods: A total of 21 rats grouped into 3(control, acute and chronic exposure groups, with all consisting of 7 rats each) was used. The acute and chronic exposure group were given 0.7 mg of ibuprofen orally for 1 and 21 days, respectively. Blood sample was collected via cardiac puncture then analyzed.&#x0D; Results: PT was significantly higher in both group 2 and 3 (acute and chronic exposure, respectively) than that of the control. Acute exposure group showed the highest PT rise. A PTT was not significantly different between group 2 and 3 versus the control group. Platelet count was significantly lower in both group 2 and 3than that in the control group (p&lt;0.05). Group 3 (chronic exposure) showed the lowest platelet count.&#x0D; Conclusion: Oral administration of ibuprofen affected coagulation parameters and a longer exposure reduce platelets count. A strictly prescription for this drug may be needed to prevent its indiscriminate use.

The effects of methamphetamine on gonadotropin and androgen, estrogen receptors in male rats

Objective To investigate the effects of methamphetamine on gonadotropin and testosterone receptors in male rats. Methods Acute and chronic exposure models were established by intraperitoneal injection of Methamphetamine (METH). Enzyme linked immunosorbent assay (ELISA) was performed to detect the expression of testosterone (T), estradiol (E2), Follicle stimulating hormone (FSH), luteinizing hormone (LH), progesterone (PROG), prolactin (PRL), structural changes of testicular were observed by hematoxylin and eosin (HE) staining, immunohistochemical staining (IHC) and Western blotting were performed to detect the localization and expression of androgen receptor (AR), estrogen receptor alpha (ER) estrogen receptor β (ERβ) in the testis. Results ELISA results showed that compared with control group, the concentration of T in the acute exposure group was (2.16±0.51) μg/L, which was significantly decreased (t=-2.432, P<0.05). The concentrations of T, E2, PRL and INH B in the chronic exposure group were (0.41±0.37) μg/L, (73.84±33.63) ng/L, (5.86±4.27) μg/L, and (22.52±7.19) ng/L respectively. The T, E2 and INH B in the chronic exposed group was significantly decreased compared to the control group (t=-6.211, -2.853, 2.553, P<0.05). While the PRL was significantly increased (t=2.318, P<0.05). HE staining showed that the spermatogenic cells in the METH exposure group were slightly reduced and disordered. Compared with control group, IHC and Western blotting showed that the protein expression of AR, ERxpond ERβ decreased in the testis. Conclusion The acute and chronic exposure of METH in male rats could lead to gonadotropin disorder and decreased expression of testosterone receptors AR, ERed with the chronic controt the occurrence and development of the sperm. Key words: Methamphetamine; Male reproduction; Gonadal hormone; Hormone receptor

Acute and sub-acute bisphenol-B exposures adversely affect sperm count and quality in adolescent male mice.

Bisphenol-B (BPB), an analogue of bisphenol-A is used in the plastic industry. It has been found to leach from plastic containers leading to its contamination in canned food products. Moreover, it has also been detected in human samples such as sera and urine. BPB is recognized as a potential endocrine disrupting chemical owing to its estrogenic and anti-androgenic nature. Therefore, it was pertinent to study the effect of BPB exposure during the adolescence age (5-6 weeks old) in male mice. Weekly intraperitoneal injections of 5, 10 and 15% LD50 of BPB were given for 2 weeks to acute exposure groups and for 4 weeks to sub-acute exposure groups. BPB exposure induces change in enzymatic and non-enzymatic oxidative stress markers in sperm samples. DNA damage was also observed in sperm cells on acute and sub-acute exposures. Furthermore, BPB exposure led to a marked decline in sperm count and compromised sperm morphology. Computer assisted sperm analysis (CASA) revealed a significant decrease in sperm quality and progressive motility. Thus, both the acute and sub-acute exposures of adolescent male mice to BPB adversely affect the sperms' quality, functions and morphology.

Renin-angiotensin system activation and imbalance of matrix metalloproteinase-9/tissue inhibitor of matrix metalloproteinase-1 in cold-induced stroke

AimsIn the present study, we investigated the roles of renin-angiotensin system (RAS) activation and imbalance of matrix metalloproteinase-9 (MMP-9)/tissue inhibitor of matrix metalloproteinase-1 (TIMP-1) in cold-induced stroke during chronic hypertension, as well as the protective effects of captopril and recombinant human TIMP-1 (rhTIMP-1). Main methodsRats were randomly assigned to sham; 2-kidney, 2-clip (2K-2C); 2K-2C + captopril, and 2K-2C + rhTIMP-1 groups. After blood pressure values had stabilized, each group was randomly divided into an acute cold exposure (ACE) group (12-h light at 22 °C/12-h dark at 4 °C) and a non-acute cold exposure (NACE) group (12-h light/12-h dark at 22 °C), each of which underwent three cycles of exposure. Captopril treatment was administered via gavage (50 mg/kg/d), while rhTIMP-1 treatment was administered via the tail vein (60 μg/kg/36 h). Key findingsIn the 2K-2C group, angiotensin II (AngII) and MMP-9 levels increased in both the plasma and cortex, while no such changes in TIMP-1 expression were observed. Cold exposure further upregulated AngII and MMP-9 levels and increased stroke incidence. Captopril and rhTIMP-1 treatment inhibited MMP-9 expression and activation and decreased stroke incidence in response to cold exposure. SignificanceThe present study is the first to demonstrate that cold exposure exacerbates imbalance between MMP-9 and TIMP-1 by activating the RAS, which may be critical in the initiation of stroke during chronic hypertension. In addition, our results suggest that captopril and rhTIMP-1 exert protective effects against cold-induced stroke by ameliorating MMP-9/TIMP-1 imbalance.

Golden mussel (Limnoperna fortunei) as a bioindicator in aquatic environments contaminated with mercury: Cytotoxic and genotoxic aspects

This study evaluated the Limnoperna fortunei (golden mussel) as a bioindicator of cytotoxicity and genotoxicity in aquatic environments contaminated by heavy metals. Five groups of 50 subjects each were exposed to different concentration of mercuric chloride (HgCl2) (0.001 mg/L, group I; 0.005 mg/L, group II; 0.01 mg/L, group II; 0.02 mg/L, group IV; and 0.1 mg/L, group V). The control group for both chronic and acute treatment did not receive HgCl2. For chronic exposure, the respective groups were placed in aquaria with water contaminated with the above concentrations of HgCl2. For acute exposure, the different concentrations of HgCl2 were injected into the posterior adductor muscle of the individuals belonging to the aforementioned groups. The biological matrix used in the tests was the whole body muscle. Tests (cell viability assay, alkaline comet test; enumeration of micronuclei and necrotic cells, quantification of Hg content in tissues and water, and histopathological analysis of tissues), were carried out on the 7th, 15th, and 30th treatment days or 2 h after injection. Our results demonstrated that L. fortunei showed cell damage in both chronic and acute exposure groups. Significant DNA damage was observed at both the 15th (0.1 mg/L) and 30th (0.01–0.1 mg/L) days of chronic exposure. However, in acute treatment all concentrations induced DNA breaks. The presence of necrosis increased at all concentrations tested for both acute and chronic exposure. Tissue mercury retention on the 15th day was higher than on the 30th day of exposure, while in the same period, there was a decrease in the mercury content of aquarium water. Taking the data together, it is concluded that L. fortunei as a possible bioindicator of the quality of aquatic environments.

Water‐pipe Smoke Negatively Distress Cardiovascular Biomarkers in Mice

Tobacco use is one of the main risk factors to cardiovascular diseases (CVDs) and atherosclerosis in particular. It was mis‐considered that water‐pipe smoking (WPS) is less harmful than cigarette smoking due to its flavor. Studies had shown that more than 100 million people smoke waterpipe daily. WPS contains several toxic materials such as: nicotine, carcinogens, tar, carbon monoxide and heavy metals. Thus, WPS is considered to be as one of the toxic environmental factors that should be investigated intensively. The aim of this study is to investigate the effect of WPS on several cardiovascular biological markers that may cause atherosclerosis in mice. The study also conducted to study the temporal effects of WPS on the atherosclerotic biomarkers upon short (2 weeks) and long‐term (8 weeks) exposures. Mice were exposed to WPS and heart homogenates were analyzed to elucidate the effects of WPS on matrix metalloproteinase (MMPs), endothelin‐1 (ET‐1) and, myeloperoxidase (MPO). Following protein estimation, enzyme‐linked immunosorbent assays were done to measure the levels of MMPs (isoforms 1, 3, and 9), MPO, and ET‐1 protein. Our data showed that acute exposure to WPS significantly enhances the levels of MMP‐3, MMP‐9, and MPO expressions (p&lt;0.05) compared to their corresponding control. However, the body was capable to compromise the levels for such parameters following continuous exposure for 8 weeks (p&gt;0.05). Additionally, we showed that the level of ET‐1 was significantly higher upon chronic exposure to WPS compared to both control and acute exposure groups (p&lt;0.05). In conclusion, WPS has a significant negative effect on cardiac health and the enhancement of the atherosclerotic biomarkers (MMP‐3 and 9, MPO, and ET‐1) might represent an early scavenger of compensatory efforts to maintain cardiac function after WP exposure.Support or Funding InformationThis project was supported by a grant from the Deanship of Research at Jordan University of Science and Technology (grant number 2015/249 to AR).This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Waterpipe tobacco smoke distresses cardiovascular biomarkers in mice: alterations in protein expression of metalloproteinases, endothelin and myeloperoxidase

Introduction: Tobacco use is a major risk factor of cardiovascular diseases (CVD) and atherosclerosis in particular. The use of waterpipe smoking (WPS) is increasing due to the misperception that it is less harmful than cigarette smoking due to its flavor and the use of water as a filter. Thus, research that investigates toxic effects of WPS is essential. The aim of this study was to investigate the effect of WPS on major cardiovascular biomarkers that may develop atherosclerosis in mice.Methods: BALB/c mice were exposed to WPS for either two weeks (acute exposure) or eight weeks (chronic exposure). Then, the heart tissue homogenates were analyzed to elucidate the effects of WPS on matrix metalloproteinase (MMPs: isoforms 1, 3, and 9), metallopeptidase inhibitor (TIMP1), endothelin-1 (ET-1) and myeloperoxidase (MPO) using ELISA technique.Results: Current data showed that acute exposure to WPS significantly enhanced the levels of MMP-3, MMP-9, and MPO (p < 0.05) compared to their corresponding control. However, the body was capable to restore the increased levels of these parameters following chronic exposure to WPS for 8 weeks (p > 0.05). Additionally, the levels of ET-1 were significantly higher upon chronic exposure to WPS compared to both control and acute exposure groups (p < 0.05).Conclusions: Waterpipe exposure has a significant negative effect on the cardiovascular system. The enhancement of the atherosclerotic biomarkers (MMP-3, MMP-9, MPO, and ET-1) might represent an early scavenger of compensatory efforts to maintain cardiovascular function after WPS exposure.

Effects of acute cold exposure on the expression of AQP-1 and AQP-5 in rat lung tissues

To study the effect of acute cold exposure on the expression of aquaporin-1 (AQP-1) and AQP-5 in lung tissues and the changes of ultrastructural pathological changes after cold exposure in rats. Twelve male Wistar rats were randomly divided into control group (23±2)℃ and cold (-25℃) exposure group, the exposure time was 2 h. Rectal temperatures of the rats were measured immediately after cold exposure. The ultrastructural pathological changes of pulmonary tissue were observed by transmission electronic microscope. The mRNA expression of AQP-1 and AQP-5 was measured by RT-PCR. The protein expression of AQP-1 and AQP-5 was measured by Western blot. The body core temperatures(28.07±4.15)℃ of the cold exposure group were decreased significantly compared with the control group(37.33±0.25)℃ (P<0.05). In acute cold exposure group, the main pathological changes of pulmonary ulstructure included pulmoary epithelial basement membrane thickening, and karyopyknosis of AT-I cells, and vacuolization on the cytoplasm of (AT-Ⅱ) cells. After acute cold exposure, the levels of both mRNA and potein expressions of AQP-5 were decreased significantly (P<0.05) compared with those in the control group. while AQP-1 expression level showed no statistical significance between control group and cold exposure group. There might be some cause and effect relationship between lung tissue damage by cold exposure and the levels of mRNA and potein expressions of AQP-5 decreased after acute cold exposure.