Abdus Salam Raju, Aditya Thomas Benjamin, Tristan Rutland, Luke Liu, Paul Lambrakis
{"title":"Appendicitis and COVID: cause or effect?","authors":"Abdus Salam Raju, Aditya Thomas Benjamin, Tristan Rutland, Luke Liu, Paul Lambrakis","doi":"10.1186/s42269-022-00798-w","DOIUrl":"10.1186/s42269-022-00798-w","url":null,"abstract":"<p><strong>Background: </strong>Vasculitis and phlebitis with vascular occlusion within appendix specimen is rare. Several authors have reported COVID-19 related veno-occlusive disease in hepatic pathology, but lymphoid aggregation with phlebitis is unusual in appendix specimen. We present a case with medium size venule phlebitis in an appendix of a patient recovered from COVID-19 infection.</p><p><strong>Case presentation: </strong>A 27-year-old who recently recovered from COVID-19 infection 12 weeks prior, presented with acute appendicitis, confirmed on computed tomography and operative findings. He underwent an uneventful laparoscopic appendicectomy. Histopathology showed veno-occlusive vasculitis within the appendix specimen.</p><p><strong>Conclusions: </strong>Veno-occlusive disease within the appendix is uncommon. Emerging data suggest COVID-19 infection can cause systemic vascular complications. We herein report a case of healthy patient with no past medical history with an unusual findings of medium vessels phlebitis within the appendix post COVID-19 infection.</p>","PeriodicalId":72650,"journal":{"name":"Comparative biochemistry and physiology. C: Comparative pharmacology","volume":"57 1","pages":"114"},"PeriodicalIF":0.0,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9021817/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"75423832","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Stefan Müller-Lissner, Gabrio Bassotti, Benoit Coffin, Asbjørn Mohr Drewes, Harald Breivik, Elon Eisenberg, Anton Emmanuel, Françoise Laroche, Winfried Meissner, Bart Morlion
{"title":"Opioid-Induced Constipation and Bowel Dysfunction: A Clinical Guideline.","authors":"Stefan Müller-Lissner, Gabrio Bassotti, Benoit Coffin, Asbjørn Mohr Drewes, Harald Breivik, Elon Eisenberg, Anton Emmanuel, Françoise Laroche, Winfried Meissner, Bart Morlion","doi":"10.1093/pm/pnw255","DOIUrl":"10.1093/pm/pnw255","url":null,"abstract":"<p><strong>Objective: </strong>To formulate timely evidence-based guidelines for the management of opioid-induced bowel dysfunction.</p><p><strong>Setting: </strong>Constipation is a major untoward effect of opioids. Increasing prescription of opioids has correlated to increased incidence of opioid-induced constipation. However, the inhibitory effects of opioids are not confined to the colon, but also affect higher segments of the gastrointestinal tract, leading to the coining of the term \"opioid-induced bowel dysfunction.\"</p><p><strong>Methods: </strong>A literature search was conducted using Medline, EMBASE, and EMBASE Classic, and the Cochrane Central Register of Controlled Trials. Predefined search terms and inclusion/exclusion criteria were used to identify and categorize relevant papers. A series of statements were formulated and justified by a comment, then labeled with the degree of agreement and their level of evidence as judged by the Strength of Recommendation Taxonomy (SORT) system.</p><p><strong>Results: </strong>From a list of 10,832 potentially relevant studies, 33 citations were identified for review. Screening the reference lists of the pertinent papers identified additional publications. Current definitions, prevalence, and mechanism of opioid-induced bowel dysfunction were reviewed, and a treatment algorithm and statements regarding patient management were developed to provide guidance on clinical best practice in the management of patients with opioid-induced constipation and opioid-induced bowel dysfunction.</p><p><strong>Conclusions: </strong>In recent years, more insight has been gained in the pathophysiology of this \"entity\"; new treatment approaches have been developed, but guidelines on clinical best practice are still lacking. Current knowledge is insufficient regarding management of the opioid side effects on the upper gastrointestinal tract, but recommendations can be derived from what we know at present.</p>","PeriodicalId":72650,"journal":{"name":"Comparative biochemistry and physiology. C: Comparative pharmacology","volume":"96 1","pages":"1837-1863"},"PeriodicalIF":0.0,"publicationDate":"2017-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5914368/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"75621271","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Naofumi Kitabatake, Etsushiro Doi, Alka B. Trivedi
{"title":"Toxicity evaluation of the mycotoxins, citrinin and ochratoxin a, using several animal cell lines","authors":"Naofumi Kitabatake, Etsushiro Doi, Alka B. Trivedi","doi":"10.1016/0742-8413(93)90082-V","DOIUrl":"10.1016/0742-8413(93)90082-V","url":null,"abstract":"<div><p>1. The cytotoxicities of the nephrotoxic mycotoxins, citrinin and ochratoxin A were assayed on HeLa, C3H/10T1/2, NIH/3T3, MDCK (canine kidney), and HeLa P3 cell lines, using the MTT colorimetric assay.</p><p>2. Citrinin was less toxic than ochratoxin A in all of the cell lines examined.</p><p>3. The MDCK cells were more susceptible to both citrinin and ochratoxin A, in comparison with other cell lines.</p><p>4. Dose-responses, as measured by activities of leucine aminopeptidase and alkaline phosphatase of MDCK cells, were less sensitive than MTT colorimetric assay, indicating that these enzymes were not specifically inhibited in MDCK cells.</p><p>5. The <span>ld</span><sub>50</sub> of both toxins, calculated at 72 hr of incubation, was in the same order as those reported from animal experiments using rats and mice.</p></div>","PeriodicalId":72650,"journal":{"name":"Comparative biochemistry and physiology. C: Comparative pharmacology","volume":"105 3","pages":"Pages 429-433"},"PeriodicalIF":0.0,"publicationDate":"1993-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/0742-8413(93)90082-V","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18901040","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
M. Bagchi, E. Hassoun, P. Akubue, D. Bagchi, S.J. Stohs
{"title":"Comparative effects of endrin on hepatic lipid peroxidation and DNA damage, and nitric oxide production by peritoneal macrophages from C57BL/6J and DBA/2 mice","authors":"M. Bagchi, E. Hassoun, P. Akubue, D. Bagchi, S.J. Stohs","doi":"10.1016/0742-8413(93)90096-4","DOIUrl":"10.1016/0742-8413(93)90096-4","url":null,"abstract":"<div><p>1. Endrin is a polyhalogenated cyclic hydrocarbon which produces hepatic and neurologic toxicity. In order to further assess the mechanism of toxicity ofendrin, the dose-dependent effects of endrin on hepatic lipid peroxidation and DNA damage, and nitric oxide (NO) production by peritoneal exudate cells (primarily macrophages) were investigated in C57BL/6J and DBA/2 mice which vary at the Ah receptor genetic locus. C57BL/6J mice are dioxin-responsive, while DBA/2 mice are dioxin-insensitive.</p><p>2. Mice of both strains were treated with 0, 1, 2 or 4 mg endrin kg<sup>−1</sup> as a single oral dose in corn oil, and the animals were killed 24 hr post-treatment. At doses of 1,2 and 4 mg endrin kg<sup>−1</sup> in C57BL/6J mice, hepatic mitochondrial lipid peroxidation increased 1.2-, 2.2- and 3.2-fold, respectively, and 1.8-, 2.3- and 3.5-fold with microsomes, respectively. At these same doses in DBA/2 mice, hepatic mitochondrial lipid peroxidation increased 1.3-, 2.0- and 2.6-fold, respectively, and 1.5-, 1.9- and 2.5-fold with microsomes, respectively.</p><p>3. Increases of 2.3-, 2.4- and 4.9-fold were observed in hepatic DNA damage (elution constants) in C57BL/6J mice at doses of 1, 2 and 4 mg endrin kg<sup>−1</sup>, respectively, while at these same three doses, increases of 1.9-, 2.1- and 2.3-fold were observed for DBA/2 mice, respectively.</p><p>4. Nitric oxide production by peritoneal macrophages from C57BL/6J increased by 1.3-, 1.7- and 2.0-fold with doses of 1, 2 and 4 mg endrin kg<sup>−1</sup>, respectively, while in macrophages from DBA/2 mice at these same doses, increases of 1.7-, 1.7- and 1.8-fold, respectively, were observed.</p><p>5. The results indicate that the responsiveness of peritoneal macrophages with respect to both DNA damage and nitric oxide production are more dose-dependent in C57BL/6J mice as compared to DBA/2 mice, while similar results are observed with the lipid peroxidation of hepatic mitochondria and microsomes of the two mouse strains. The results suggest that the toxicity of endrin is less reliant on a mechanism which may involve the Ah receptor system as compared to dioxins as 2,3,7,8-tetrachlorodibenzo-<em>p</em>-dioxin (TCDD).</p></div>","PeriodicalId":72650,"journal":{"name":"Comparative biochemistry and physiology. C: Comparative pharmacology","volume":"105 3","pages":"Pages 525-529"},"PeriodicalIF":0.0,"publicationDate":"1993-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/0742-8413(93)90096-4","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18901046","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Bioaccumulative potential and toxicity of endosulfan insecticide to non-target animals","authors":"Syed M. Naqvi , Chetana Vaishnavi","doi":"10.1016/0742-8413(93)90071-R","DOIUrl":"10.1016/0742-8413(93)90071-R","url":null,"abstract":"<div><p>1. Endosulfan insecticide is a polychlorinated compound used for controlling a variety of insects; it is practically water-insoluble, but readily adheres to clay particles and persists in soil and water for several years. Its mode of action involves repetitive nerve-discharges positively correlated to increase in temperature. This compound is extremely toxic to most fish and can cause massive mortalities. In fish, it causes marked changes in Na and K concentrations, decrease in blood Ca<sup>2+</sup> and Mg levels and inhibits Na, K and Mg-dependent ATPase (in brain).</p><p>2. Bioaccumulation of endosulfan is reported for marine animals; however, freshwater animals (e.g. crayfish) accumulate it to some extent, but they lose the compound rapidly during depuration. Endosulfan is generally less toxic to aquatic invertebrates than fish. However, it causes decreases in adenylate energy charge, oxygen consumption, hemolymph amino acids, succinate dehydrogenase, heart-beat (mussel) and altered osmoregulation.</p><p>3. Generally, mammals are less susceptible to endosulfan's toxicity than aquatic animals. The majority of studies conducted on laboratory mammals can be summarized, (a) Neurotoxicity: male rats are more sensitive than females to endosulfan, which decreases brain and plasma acetyleholinesterase activity. Endosulfan I (a metabolite) causes a significant change in norepinephrine, 5-HT and GABA. (b) Renal toxicity: inhibition of MFOs activity was noticed in rats; other effects included changes in proximal convoluted tubules and necrosis of the tubular epithelium, (c) Hepatotoxicity: chemically-induced aminopyrine <em>N</em>-demethylase and aniline hydrolase were found in rat liver, and reduction in the glycogen level occurred, (d) Hematologic toxicity: endosulfan exposure resulted in a significant decrease in the erythrocyte glutathione reductase, hemoglobin amount, RBC number and mean corpuscular volume.</p><p>4. Respiratory toxicity: involved dyspnea, acute emphysema, cyanosis and hemorrhages in the interalveolar partitions of rat's lungs.</p><p>5. Biochemical: in rats, endosulfan caused increased glucose-6-phosphate dehydrogenase activity, blood glucose level, phospholipid contents of the microsomal and surfactant system, and profoundly induced the activity of alcohol dehydrogenase and cytosolic glutathione S-transferases. It also decreased significantly Na<sup>+</sup>, K<sup>+</sup> and Mg<sup>2+</sup> ATPases, plasma calcium level and alkaline phosphatase in the intestinal epithelium.</p><p>6. Immunologic toxicity: rat serum antibody titer to tetanus toxin, IgG, IgM and gammaglobulins were significantly reduced.</p><p>7. Reproductive toxicity: degenerative changes in the seminiferous epithelium, induction of the rate-limiting enzyme in testosterone production (3β-hydroxysteroid transferase and 17β-hydroxysteroid transferase), histological changes in reproductive organs, testicular atrophy and the occurrence of ovarian cysts were notic","PeriodicalId":72650,"journal":{"name":"Comparative biochemistry and physiology. C: Comparative pharmacology","volume":"105 3","pages":"Pages 347-361"},"PeriodicalIF":0.0,"publicationDate":"1993-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/0742-8413(93)90071-R","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18897671","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Calcium dependence of electrical and mechanical activity in rat ileum examined by the sucrose-gap technique","authors":"S.M. Mahmod , H. Huddart","doi":"10.1016/0742-8413(93)90075-V","DOIUrl":"10.1016/0742-8413(93)90075-V","url":null,"abstract":"<div><p>1. Single sucrose gap recordings showed that spontaneous action potentials of rat ileal smooth muscle consisted of slow waves and superimposed spikes which generated rhythmic contractions. As external potassium was raised, the resting potential progressively depolarized.</p><p>2. Calcium-free salines inhibited spontaneous mechanical activity and inhibited the plateau phase of the action potential, but spontaneous spike depolarizations persisted.</p><p>3. Verapamil, nifedipine and diltiazem all inhibited spontaneous mechanical activity and the plateau phase of the action potential, while in addition diltiazem augmented spike amplitude.</p><p>4. Mn ions also inhibited mechanical activity and the action potential plateau, without affecting spike activity while the calcium ionophore A23187 enhanced both mechanical and electrical activity with a pronounced effect on spike amplitude.</p><p>5. These results are consistent with the view that the plateau phase of the ileal smooth muscle action potential is dependent upon an influx of extracellular calcium possibly through voltage dependent slow calcium channels.</p></div>","PeriodicalId":72650,"journal":{"name":"Comparative biochemistry and physiology. C: Comparative pharmacology","volume":"105 3","pages":"Pages 387-391"},"PeriodicalIF":0.0,"publicationDate":"1993-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/0742-8413(93)90075-V","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18897673","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Brenda Oppert, Thomas D. Morgan, Christina Culbertson, Karl J. Kramer
{"title":"Dietary mixtures of cysteine and serine proteinase inhibitors exhibit synergistic toxicity toward the red flour beetle, Tribolium castaneum","authors":"Brenda Oppert, Thomas D. Morgan, Christina Culbertson, Karl J. Kramer","doi":"10.1016/0742-8413(93)90074-U","DOIUrl":"10.1016/0742-8413(93)90074-U","url":null,"abstract":"<div><p>1. Combinations of a cysteine proteinase inhibitor (CPI) and serine proteinase inhibitors (SPI) in wheat germ diets were toxic to larvae of the red flour beetle, <em>Tribolium castaneum</em>, when tested at levels where individual inhibitors were nontoxic.</p><p>2. Mixtures of 0.1% (w/w) CPI (E-64) plus 1% of either of three plant SPIs (soybean Kunitz trypsin inhibitor, soybean Bowman-Birk trypsin-chymotrypsin inhibitor, or lima bean trypsin inhibitor) inhibited <em>T. castaneum</em> growth, resulting in 82–97% reduction in larval weight gain 17 days after hatching and 40–60% mortality.</p><p>3. Supplemention of diet containing 0.1% E-64 plus 1% soybean Kunitz trypsin inhibitor (STI) with a mixture of amino acids at 7% caused a partial reversal of the growth inhibition, with 91% of the larvae surviving.</p><p>4. Diet containing 0.1% E-64 plus either 5 or 10% STI resulted in 100% mortality of the larvae during the first or second instar.</p><p>5. Addition of a mixture ofamino acids at 20% to the 0.1% E-64 plus 10% STI diet allowed 89% of the larvae to develop into adults.</p><p>6. The synergism between different classes of proteinase inhibitors in the insect's diet that enhances growth inhibition and toxicity demonstrates the potential for an insect pest management strategy involving the coordinated manipulation of two or more types of digestive enzyme inhibitor genes in plants.</p></div>","PeriodicalId":72650,"journal":{"name":"Comparative biochemistry and physiology. C: Comparative pharmacology","volume":"105 3","pages":"Pages 379-385"},"PeriodicalIF":0.0,"publicationDate":"1993-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/0742-8413(93)90074-U","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"54006307","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Diacylglycerol: Formation and function in phospholipid-mediated signal transduction","authors":"E.W. Haeffner","doi":"10.1016/0742-8413(93)90070-2","DOIUrl":"10.1016/0742-8413(93)90070-2","url":null,"abstract":"<div><p>1. Properties, distribution and multiplicity of phosphoinositidases (phospholipase C, PLC) are investigated.</p><p>2. Generation of diacylglycerol (DAG) by a variety of enzymes such as phosphoinositide and phosphatidylcholine specific PLC, by a combination of phospholipase D and phosphatidic hydrolase, and by triglyceride lipase is examined.</p><p>3. Ca<sup>2+</sup> and phospholipid-dependent protein kinase C act as the target of DAG messenger action.</p><p>4. There are differences in the formation of DAG in normal and transformal cell.</p></div>","PeriodicalId":72650,"journal":{"name":"Comparative biochemistry and physiology. C: Comparative pharmacology","volume":"105 3","pages":"Pages 337-345"},"PeriodicalIF":0.0,"publicationDate":"1993-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/0742-8413(93)90070-2","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18897028","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
P. Kerambrun , M. Thessalou-Legaki , G. Verriopoulos
{"title":"Comparative effects of environmental conditions, in eutrophic polluted and oligotrophic non-polluted areas of the saronikos gulf (Greece), on the physiology of the copepod Acartia clausi","authors":"P. Kerambrun , M. Thessalou-Legaki , G. Verriopoulos","doi":"10.1016/0742-8413(93)90080-5","DOIUrl":"10.1016/0742-8413(93)90080-5","url":null,"abstract":"<div><p>1. Digestive enzyme activity and the oxygen consumption rate of <em>Acartia clausi</em> from the polluted eutrophic Elefsis Bay and the non-polluted oligotrophic Vouliagmeni-Fleves area were compared.</p><p>2. Out of 13 hydrolases whose activity was revealed, 10 had a higher activity in the Elefsis population than in the Vouliagmeni-Fleves one. Only amylase, alkaline phosphatase and esterase lipase had a higher activity in the Vouliagmeni-Fleves population.</p><p>3. The high activity of amylase in Vouliagmeni-Fleves population seems to indicate that phytoplankton constitutes the most important part of <em>A. clausi's</em> food.</p><p>4. Respiration rate was significantly lower in Elefsis population, irrespective of season.</p><p>5. A significant seasonal variation was observed which was greater in the Vouliagmeni-Fleves population, with a 50% decrease in the respiration rate between spring and summer.</p><p>6. The obtained results agree with previous literature data and show the physiological characteristics of <em>A. clausi</em> of Elefsis Bay, allowing it to thrive in polluted eutrophic waters.</p></div>","PeriodicalId":72650,"journal":{"name":"Comparative biochemistry and physiology. C: Comparative pharmacology","volume":"105 3","pages":"Pages 415-420"},"PeriodicalIF":0.0,"publicationDate":"1993-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/0742-8413(93)90080-5","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"54006363","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Effect of diesel fuel hydrocarbons on embryogenesis and 45Ca2+ uptake by unfertilized eggs of sea urchin, Strongylocentrotus intermedius","authors":"P.M. Zhadan , M.A. Vaschenko","doi":"10.1016/0742-8413(93)90099-7","DOIUrl":"10.1016/0742-8413(93)90099-7","url":null,"abstract":"<div><p>1. The quality of unfertilized eggs of the sea urchin <em>Strongylocentrotus intermedius</em>, kept for a long time (50 days) in a sea water containing water soluble hydrocarbons of diesel fuel in sublethal concentrations (0.3–0.04 mg/l), was assessed through observation of embryogenesis and the intensity of <sup>45</sup>Ca<sup>2+</sup> uptake.</p><p>2. It has been shown that such treatment led to delay and asynchronism of embryonal and larval development and to appearance of a greater number of abnormalities compared to the control.</p><p>3. Unfertilized eggs of sea urchins exposed to the hydrocarbons in sublethal concentrations accumu- lated 30–60% more <sup>45</sup>Ca<sup>2+</sup> than those of control animals. Short-term incubation (2 hr) of eggs at the same hydrocarbon concentrations did not change <sup>45</sup>Ca<sup>2+</sup> uptake by unfertilized eggs of control animals.</p><p>4. The increase of hydrocarbon concentration up to 1 mg/l (i.e. to a concentration causing disturbance of embryogenesis in acute experiments) in short-term experiments caused a small elevation in the <sup>45</sup>Ca<sup>2+</sup> uptake by unfertilized eggs of control animals (30% more than in untreated eggs).</p><p>5. Ionomycin-induced (concentration 10<sup>−8</sup>−10<sup>−9</sup>) increase of <sup>45</sup>Ca<sup>2+</sup> uptake by unfertilized eggs (50–100% more than the untreated eggs) caused the same disturbance of embryogenesis as under hydrocarbon exposure.</p><p>6. It is suggested that one of the mechanisms inducing the deleterious effect of hydrocarbons in sea urchin gametes is related to the increase of membrane permeability to calcium ions.</p></div>","PeriodicalId":72650,"journal":{"name":"Comparative biochemistry and physiology. C: Comparative pharmacology","volume":"105 3","pages":"Pages 543-548"},"PeriodicalIF":0.0,"publicationDate":"1993-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/0742-8413(93)90099-7","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"54006571","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}