scholarly journals Physiological and metabolic alterations induced by commercial neonicotinoid formulations in Daphnia magna

2021 ◽  
Author(s):  
Anna Farkas ◽  
Dávid Somogyvári ◽  
Attila W. Kovács ◽  
Mária Mörtl ◽  
András Székács ◽  
...  
Keyword(s):  
Heart Rate ◽  
Daphnia Magna ◽  
Insect Pests ◽  
Fold Increase ◽  
Monooxygenase System ◽  
Aquatic Biota ◽  
P450 Monooxygenase ◽  
Thoracic Limb ◽  
Significant Depression ◽  
Neonicotinoid Pesticides

Abstract Neonicotinoid insecticides are widely used agents in agriculture to control a broad range of insect pests. Although use of neonicotinoid pesticides has resulted in the widespread contamination of surface waters, sublethal toxicity data of these products in relation to non-target aquatic biota are still poor. Therefore, the objective of this study was to assess the effects of two neonicotinoid pesticides with widespread use on the basic physiological functions: the thoracic limb activity and heart rate of Daphnia magna, and to screen for their potential to affect the cytochrome P450 monooxygenase system of daphnids. The considered pesticides were the acetamiprid- and thiacloprid based products Mospilan 20 SG and Calypso 480 SC. The dose-dependent variation in the three biological endpoints considered were assessed following 24h exposures. The two neonicotinoid formulations elicited significant depression on the thoracic limb activity and heart rate of daphnids at doses close to the 48h-EC50 of the products, a response mainly attributable to the overall drop in the general health status of the organisms. The dose related variation in the ECOD activity of daphnids exposed to the selected neonicotinoid formulations followed a biphasic pattern, with starting effective doses for Mospilan 20 SG of 6.3 mg L-1 (= 1/20 of 48h-EC50 for Daphnia neonates), and for Calypso 480 SC of 0.034 mg L-1 (= 1/4000 of 48h-EC50). Maximal ECOD activity (2.2 fold increase vs. controls) was induced by Mospilan 20 SG in daphnids exposed to 114 mg L-1 product (= 48h-EC20), and by Calypso 480 SC (1.8 fold increase) at 5.2 mg L-1 dose (= 1/20 of 48h-EC50). The results outlined significant alterations in the physiological traits considered at concentrations below the immobility thresholds (48h-EC50) of the products used as benchmarks to rate their toxicity risks to aquatic biota. Therefore, we think our findings might deserve consideration in the environmental risk evaluation of these products.

Protein-Protein Interactions in the P450 Monooxygenase System

1999 ◽  
pp. 21-39
Author(s):  
John B. Schenkman ◽  
Ingela Jansson ◽  
Gary Davis ◽  
Paul P. Tamburini ◽  
Zhongqing Lu ◽  
...  
Keyword(s):  
Protein Interactions ◽  
Monooxygenase System ◽  
Protein Protein Interactions ◽  
P450 Monooxygenase

Cardiovascular changes in the exercising emu

1983 ◽  
Vol 104 (1) ◽  
pp. 193-201 ◽  
Author(s):  
B. Grubb ◽  
D. D. Jorgensen ◽  
M. Conner
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Oxygen Consumption ◽  
Stroke Volume ◽  
Oxygen Content ◽  
Body Mass ◽  
Fold Increase ◽  
Exercise Heart Rate ◽  
Rate Of Oxygen Consumption ◽  
Cardiovascular Variables

Cardiovascular variables were studied as a function of oxygen consumption in the emu, a large, flightless ratite bird well suited to treadmill exercise. At the highest level of exercise, the birds' rate of oxygen consumption (VO2) was approximately 11.4 times the resting level (4.2 ml kg-1 min-1). Cardiac output was linearly related to VO2, increasing 9.5 ml for each 1 ml increase in oxygen consumption. The increase in cardiac output is similar to that in other birds, but appears to be larger than in mammals. The venous oxygen content dropped during exercise, thus increasing the arteriovenous oxygen content difference. At the highest levels of exercise, heart rate showed a 3.9-fold increase over the resting rate (45.8 beats min-1). The mean resting specific stroke volume was 1.5 ml per kg body mass, which is larger than shown by most mammals. However, birds have larger hearts relative to body mass than do mammals, and stroke volume expressed per gram of heart (0.18 ml g-1) is similar to that for mammals. Stroke volume showed a 1.8-fold increase as a result of exercise in the emus, but a change in heart rate plays a greater role in increasing cardiac output during exercise.

scholarly journals Extreme bradycardia and tachycardia in the world’s largest animal

2019 ◽  
Vol 116 (50) ◽  
pp. 25329-25332 ◽  
Author(s):  
J. A. Goldbogen ◽  
D. E. Cade ◽  
J. Calambokidis ◽  
M. F. Czapanskiy ◽  
J. Fahlbusch ◽  
...  
Keyword(s):  
Heart Rate ◽  
Large Diameter ◽  
Large Body ◽  
Fold Increase ◽  
Oxygen Depletion ◽  
Blue Whale ◽  
Heart Rates ◽  
Physiological Limits ◽  
Low Mass ◽  
Lunge Feeding

The biology of the blue whale has long fascinated physiologists because of the animal’s extreme size. Despite high energetic demands from a large body, low mass-specific metabolic rates are likely powered by low heart rates. Diving bradycardia should slow blood oxygen depletion and enhance dive time available for foraging at depth. However, blue whales exhibit a high-cost feeding mechanism, lunge feeding, whereby large volumes of prey-laden water are intermittently engulfed and filtered during dives. This paradox of such a large, slowly beating heart and the high cost of lunge feeding represents a unique test of our understanding of cardiac function, hemodynamics, and physiological limits to body size. Here, we used an electrocardiogram (ECG)-depth recorder tag to measure blue whale heart rates during foraging dives as deep as 184 m and as long as 16.5 min. Heart rates during dives were typically 4 to 8 beats min−1 (bpm) and as low as 2 bpm, while after-dive surface heart rates were 25 to 37 bpm, near the estimated maximum heart rate possible. Despite extreme bradycardia, we recorded a 2.5-fold increase above diving heart rate minima during the powered ascent phase of feeding lunges followed by a gradual decrease of heart rate during the prolonged glide as engulfed water is filtered. These heart rate dynamics explain the unique hemodynamic design in rorqual whales consisting of a large-diameter, highly compliant, elastic aortic arch that allows the aorta to accommodate blood ejected by the heart and maintain blood flow during the long and variable pauses between heartbeats.

Hemodynamic effects of vasopressin compared with angiotensin II in conscious rats

1987 ◽  
Vol 252 (3) ◽  
pp. H628-H637 ◽  
Author(s):  
J. W. Osborn ◽  
M. M. Skelton ◽  
A. W. Cowley
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Angiotensin Ii ◽  
Arterial Pressure ◽  
Peripheral Resistance ◽  
Fold Increase ◽  
Adrenergic Blockade ◽  
Ganglionic Blockade ◽  
Conscious Rats ◽  
Potent Vasoconstrictor

The mechanisms whereby arginine vasopressin influences hemodynamic and autonomic function were investigated in conscious rats. In normal rats, 60-min intravenous infusions produced dose-related increases of arterial pressure and total peripheral resistance with marked decreases of both heart rate and cardiac output. Cholinergic blockade with methscopolamine attenuated the bradycardia at higher doses of vasopressin, whereby the fall of cardiac output was not affected. beta-Adrenergic blockade with atenolol attenuated the fall of heart rate seen with lower doses of vasopressin but did not prevent the fall of cardiac output. Ganglionic blockade with methscopolamine and hexamethonium resulted in nearly a 60-fold enhancement of vasopressin pressor sensitivity. This was related to a greater rise of peripheral resistance, since the fall of cardiac output was not altered compared with normal rats. Hemodynamic responses to angiotensin II were determined in other groups of conscious, normal rats and rats with ganglionic blockade. Peripheral resistance increased in the normal rats, whereas the related decreases in cardiac output and heart rate were only 30% of the responses seen with equipressor doses of vasopressin. Ganglionic blockade increased pressor activity only two- to eightfold compared with the 60-fold increase observed with vasopressin. We conclude that vasopressin is a more potent vasoconstrictor than angiotensin II, decreases cardiac output independent of neural mechanisms, and results in withdrawal of sympathetic vascular tone to buffer rises of arterial pressure.

Propranolol induces acute natriuresis by β blockade and dopaminergic stimulation

1976 ◽  
Vol 54 (5) ◽  
pp. 683-691 ◽  
Author(s):  
M. C. Carrara ◽  
A. D. Baines
Keyword(s):  
Heart Rate ◽  
Sodium Excretion ◽  
Fold Increase ◽  
Nerve Function ◽  
Distal Nephron ◽  
Salt Diet ◽  
Blocking Effects ◽  
Low Salt ◽  
Dopaminergic Stimulation ◽  
Postganglionic Nerve

dl-Propranolol (0.8–1.6 mg/kg∙h for 1 h) produced a transient two- to three-fold increase in sodium excretion in nondiuretic rats infused with Pitressin and aldosterone and in water diuretic rats. Sodium excretion increased more in rats depleted of renin by chronic Doca and salt administration than in rats maintained on a low salt diet. An angiotensin inhibitor (1,sarcosine-8,valine angiotensin II) decreased sodium excretion. Therefore the natriuresis was not mediated by antidiuretic hormone, aldosterone, or renin–angiotensin. d-Propranolol did not produce a natriuresis. Prior treatment with phenoxybenzamine did not prevent the natriuretic response but chlorisondamine pretreatment did. The natriuresis is produced by β blockade and requires postganglionic nerve function but is independent of α receptors. dl-Propranolol decreased heart rate and cardiac output but systemic pressure did not fall and renal blood flow increased. This suggests a dopamine-mediated renal vasodilation and natriuresis. Haloperidol and pimozide, both dopamine blocking agents with minimal β blocking effects, prevented the natriuretic response. We conclude that propranolol may increase sodium excretion directly by blocking β receptors in the distal nephron and indirectly by dopamine-mediated renal vasodilation.

scholarly journals Purification of Cytochrome P450 and Ferredoxin, Involved in Bisphenol A Degradation, from Sphingomonas sp. Strain AO1

2005 ◽  
Vol 71 (12) ◽  
pp. 8024-8030 ◽  
Author(s):  
Miho Sasaki ◽  
Ayako Akahira ◽  
Ko-ichi Oshiman ◽  
Tetsuaki Tsuchido ◽  
Yoshinobu Matsumura
Keyword(s):  
Mass Spectrometry ◽  
Cytochrome P450 ◽  
Bisphenol A ◽  
Cytochrome P450 Monooxygenase ◽  
Mass Spectrometry Analysis ◽  
Monooxygenase System ◽  
P450 Monooxygenase ◽  
Monooxygenase Activity ◽  
Chromatography Analysis ◽  
Ferredoxin Reductase

ABSTRACT In a previous study (M. Sasaki, J. Maki, K. Oshiman, Y. Matsumura, and T. Tsuchido, Biodegradation 16:449-459, 2005), the cytochrome P450 monooxygenase system was shown to be involved in bisphenol A (BPA) degradation by Sphingomonas sp. strain AO1. In the present investigation, we purified the components of this monooxygenase, cytochrome P450 (P450bisd), ferredoxin (Fdbisd), and ferredoxin reductase (Redbisd). We demonstrated that P450bisd and Fdbisd are homodimeric proteins with molecular masses of 102.3 and 19.1 kDa, respectively, by gel filtration chromatography analysis. Spectroscopic analysis of Fdbisd revealed the presence of a putidaredoxin-type [2Fe-2S] cluster. P450bisd, in the presence of Fdbisd, Redbisd, and NADH, was able to convert BPA. The Km and k cat values for BPA degradation were 85 ± 4.7 μM and 3.9 ± 0.04 min−1, respectively. NADPH, spinach ferredoxin, and spinach ferredoxin reductase resulted in weak monooxygenase activity. These results indicated that the electron transport system of P450bisd might exhibit strict specificity. Two BPA degradation products of the P450bisd system were detected by high-performance liquid chromatography analysis and were thought to be 1,2-bis(4-hydroxyphenyl)-2-propanol and 2,2-bis(4-hydroxyphenyl)-1-propanol based on mass spectrometry-mass spectrometry analysis. This is the first report demonstrating that the cytochrome P450 monooxygenase system in bacteria is involved in BPA degradation.

Heart Rate Characteristics Monitoring in the NICU

2012 ◽  
pp. 175-200
Author(s):  
Karen D. Fairchild ◽  
J. Randall Moorman
Keyword(s):  
Heart Rate ◽  
Very Low Birth Weight ◽  
Clinical Care ◽  
Clinical Signs ◽  
Vital Signs ◽  
Signs And Symptoms ◽  
Fold Increase ◽  
Preterm Neonates ◽  
Low Birth Weight Infants ◽  
Clinical Signs And Symptoms

Heart rate variability (HRV), a marker of autonomic nervous system function, is depressed in sepsis and other acute and chronic diseases. Preterm neonates with sepsis have been shown to have both depressed HRV and repetitive transient heart rate decelerations. These abnormal heart rate characteristics (HRC) of depressed variability and decelerations may precede other clinical signs and symptoms of sepsis and usually are not apparent to clinicians using conventional vital signs monitoring. In order to quantitate these changes associated with sepsis, a heart rate characteristics monitor was developed which continuously calculates an HRC index from the conventional electrocardiogram waveform tracing. This HRC index is the fold-increase in risk that a baby will experience a clinical deterioration consistent with proven or clinical sepsis in the next 24 hours. This HRC or HeRO™ (Heart Rate Observation) Monitor can alert clinicians to carefully evaluate a patient and consider antibiotic therapy or other interventions. The impact of continuous HRC monitoring on outcomes of preterm infants was the subject of a multicenter randomized clinical trial of 3003 very low birth weight infants, completed in 2010, which showed a significant reduction in mortality in neonates whose HRC index, or “HeRO Score” was displayed to clinicians in the NICU. Continuous HRC monitoring is an important new tool for both clinical care and research in the NICU.

Abstract P470: Cardiac Autonomic Neuropathy Develops As A Result Of Mild Hypercaloric Intake In Absence Of Signs Of Diabetes: Modulation By Anti-diabetic Drugs.

Hypertension ◽  
2017 ◽  
Vol 70 (suppl_1) ◽  
Author(s):  
Ahmed El-Yazbi ◽  
Ola Al-Assi ◽  
Rana Ghali ◽  
Abdullah Kaplan ◽  
Nahed Mougharbil ◽  
...  
Keyword(s):  
Heart Rate ◽  
Autonomic Neuropathy ◽  
Pressor Response ◽  
Fold Increase ◽  
Cardiovascular Complications ◽  
Frequency Domain Analysis ◽  
Cardiac Autonomic Neuropathy ◽  
Oral Glucose ◽  
Diabetic Patients ◽  
Risk Predictor

Cardiac autonomic neuropathy (CAN) represents a major cause of morbidity and mortality in diabetes. It is usually seen early in the course of diabetes as an impaired heart rate variability (HRV) and baroreflex sensitivity (BRS), and represents an independent risk predictor of cardiac mortality. CAN development is linked to hyperglycemia; however, current understanding extends cardiovascular risk to pre-diabetic patients with slight glycemic changes. As well, recent evidence suggests that anti-diabetic drugs (metformin and pioglitazone) reduced the risk of cardiovascular complications in pre-diabetic patients. Here, we assessed whether CAN develops independent of hyperglycemia and whether metformin or pioglitazone modify this process. Rats were fed a hypercaloric (HC) diet (4.035 KCal/g vs. 3 KCal/g for control rats) composed of: weight (calories) 18.06 % fat (38.68%), 15.8% protein (15.66%), and 46.13% carbohydrates (45.73%). Stable fasting hyperglycemia developed by 16 weeks of feeding. However, at 12 weeks of feeding, there was no elevation in body weight, fasting or random blood glucose, and no difference in oral glucose tolerance, yet an increase in adipose inflammatory cytokines was observed (4- and 40- fold increase in IL-1β and TGF-β expression). No change in systolic blood pressure was observed over the course of feeding. At 12 weeks, carotid and jugular access were established. Mean arterial pressure (MAP) and heart rate (HR) were recorded, and BRS was assessed using Oxford method. HC-fed rats had a higher pressor response to increasing i.v. doses of phenylephrine vs. control rats. BRS sensitivity was blunted (slope of the ΔMAP vs. ΔHR line, -1.018 ± 0.1217 vs. -0.3379 ± 0.04135) indicating reduced parasympathetic feedback. A 2-week treatment with pioglitazone (2.5 mg/Kg) or metformin (100 mg/Kg) normalized the adipose cytokine profile, yet only pioglitazone improved BRS (-0.7463 ± 0.05775). Parasympathetic dysfunction in HC fed rats was further demonstrated by a decreased high frequency power upon frequency domain analysis of HRV data (3098 ± 233 vs. 89 ± 88 μs 2 ). To our knowledge, this is the first report that CAN occurs prior to any glycemic alterations with a potential role for adipose inflammation and modification by antidiabetic drugs.

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