Abstract
Since fish hearts are resistant to the effects of hypoxia, comparison of the effects of hypoxia and ischaemia on fish and mammalian hearts may lead to better understanding of ischaemic injury in mammalian hearts. The ultrastructure and levels of ATP, creatine phosphate, and lactic acid were examined in hearts obtained from largemouth bass. Bass hearts were subjected to conditions of normoxia, ischaemia, hypoxia, and hypoxia in the presence of fluoride and cyanide. ATP levels remained stable during hypoxia and ischaemia, but fell during hypoxia in the presence of fluoride or fluoride plus cyanide. Changes in creatine phosphate and lactic acid indicated ATP was produced during hypoxia and ischaemia by glycolysis, by rephosphorylation from creatine phosphate, and by oxidative phosphorylation with oxygen obtained from myoglobin or the atmosphere. Ultrastructural changes were found similar to those reported in ischaemic mammalian heart, consisting of inter- and intracellular swelling, glycogen depletion, and mitochondrial alterations. Comparison of metabolic rates between fish and mammalian hearts suggests the lower rate in fish hearts may be the chief factor which permits stable ATP levels during hypoxia and ischaemia, and thus provides resistance to these conditions.
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Fluoride in low concentration modifies expression and activity of 15 lipoxygenase in human PBMC differentiated monocyte/macrophage
Epidemiological and experimental evidences demonstrate positive correlation between environmental and occupational fluoride exposure and risk to various cardio-respiratory disorders. Therefore we decided to examine the effect of fluorides on activity and expression of 15LOX enzyme which is implicated in biosynthesis of inflammatory mediators. Expression of 15LOX-1 and -2 enzymes mRNA
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Risk of ischemic heart disease among primary aluminum production workers.
The risk of ischemic heart disease (IHD) has been studied in relation to working conditions encountered in a primary aluminum smelter employing over 6,000 men. During the period 1975-1983, 306 new cases of IHD were identified which were matched with 575 referents. A logistic regression analysis was performed to adjust
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Ca2+ metabolic disorder and abnormal expression of cardiac troponin involved in fluoride-induced cardiomyocyte damage.
Highlights F induced cardiomyocyte damage. F induced Ca2+ metabolic disorder. F inhibited the expression of cardiac troponin. F induced ultrastructure damage in cardiomyocytes. F interfered with production of ATP in cardiomyocytes. Our previous study indicated that excessive fluoride (F) induces ATP5J and ATP5H proactive expression by interfering cardiomyocyte mitochondrial dysfunction in
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Stimulation of cAMP accumulation in rat aorta and diaphragm by fluorine containing compounds
Evidence is presented that accumulation of cAMP in isolated rat thoracic aorta and diaphragm is stimulated by several fluorine containing compounds (NaF, Na2PO3F (MFP) and SnF2). Time course experiments with NaF showed that maximal stimulation of cAMP accumulation was observed within 2.5 min. NaF and MFP produced significant increases in
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Chronic fluorosis: the disease and its anaesthetic implications..
Abstract Chronic fluorosis is a widespread disease-related to the ingestion of high levels of fluoride through water and food. Prolonged ingestion of fluoride adversely affects the teeth, bones and other organs and alters their anatomy and physiology. Fluoride excess is a risk factor in cardiovascular disease and other major diseases, including
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Fluoride & Electrocardiogram Abnormalities
An electrocardiogram (ECG) is a diagnostic test that measures the electrical activity of the heart. An ECG can reveal heart rate, heart rhythym (i.e. steady or irregular), and the strength and timing of the heart’s natural electrical signals. ECGs are described in terms of “waves” (e.g. amplitude and duration). Problems
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Fluoride & Arterial Calcification
The major change involved with cardiovascular disease is development of atherosclerosis in critical arteries, which is partially characterized by vascular calcification. The level of coronary artery calcification is thought to be the most important indicator of future cardiovascular events. Increased arterial calcifications have frequently been reported in those with skeletal fluorosis
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Fluoride & Myocardial Damage
Structural damage to the heart resulting from fluoride toxicity has been observed in numerous human and animal studies. The general features of this damage include cloudy swelling, vacuolization or vacuolar degeneration, hemorrhages, interstitial edema, fibrous necrosis, dissolution of nuclei, and thickening of the vessel walls in the heart muscle (Basha
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Fluoride, Blood Pressure and Hypertension
Individuals with blood pressure readings that exceed 140/90 are considered hypertensive. Hypertension can increase the risk of stroke, heart attack, heart failure, aortic aneurysms, and peripheral arterial disease. An association between increased fluoride in ground water and increased prevalence of hypertension has been observed, especially among adult males (Amini et
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Fluoride & Arteriosclerosis
Healthy arteries are flexible and elastic, allowing efficient transfer of blood and nutrients from the heart to the rest of the body. Arteriosclerosis refers to a stiffening of the arteries, including loss of elasticity. This is a slow, progressive disease that may begin early in life from damage to the
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