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Animal studies on the toxicity of heavy metals have been widely used as model to simulate the impacts of environmental pollution on the human health. In the present study the authors hypothesized that cadmium exposure inducts changes in reactive oxygen species (ROS) and that may be involved in the pathogenesis of lung diseases. The pathological changes of different pulmonary cells of ROS-cadmium-dependent effects were investigated in relation to the activity of lactate dehydrogenase (LDH) and glutathione peroxidase (GPx). Twelve animals were randomly assigned to two groups, control and experimental. The experimental group underwent ingestion of cadmium mixed with diet (200 mg/kg) for 7 weeks. Following the treatment conditions for each group, blood samples were collected and animals were sacrificed and the lung was isolated. Ultrastructure examination showed that cadmium resulted in desquamated pneumocyte type II with degenerated surfactant materials, thickened alveolar wall, and thickening of alveolar septum due to proliferation of endothelial cells lining the pulmonary capillaries as a result of an active transmigration. t-test results showed that cadmium caused a significant (p < .05) rise in leukocytes, lymphocytes, neutrophils, and monocytes, which was a sign for chemotactic activity that enhanced transmigration from pulmonary microcirculation into inflammated tissue. In addition, lung tissue FR production, LDH, and GPx activities increased significantly (p < .05) from the baseline control of 88.17+/-17.70, 183.49+/-29.50, and 4466.79+/-1190.32 to 129.67+/-14.49.14 (Carr U), 339.17+/-75.28 (U/L), and 5943.08+/-695 (U/L) respectively, in the cadmium-treated group. Based on the results of the present study, it can be concluded that long-term cadmium exposure (ingestion mixed with food) results in cadmium deposition in the tissue of the vasculature of the lungs, such as pulmonary capillary endothelial, which induced the buildup of ROS, a possible proposed new mechanism that explains lung inflammation.

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ABSTRACT The purpose of this study was to examine the effects of Cerastes cerastes gasperetti crude venom (CCV) on free radical (FR) production and biological antioxidant potential (BAP). Thirty male rats, matched with age and weight, were divided randomly into three groups: control (C), negative control (NC), and experimental (E). Animals in the control group served as control for needlestick and venom injection. Animals in the negative control group, which served as control for venom-induced effects, were injected intraperitoneally (IP) with saline for 8 days, whereas animals of the experimental group were injected IP with crude CCV, at a dose of 1/4 LD(50), for the same period. All animals of the three groups remained under normal laboratory and dietary conditions. Blood samples were collected by heart puncture technique and were analyzed immediately for FRs and BAP. ANOVA analysis indicated a significant difference (p < 0.05) among group means. Tukey-Kramer multiple comparisons showed that FRs increased significantly (p < 0.05) in the NC group, implying that needlestick during injection of saline for 8 days caused internal organ injury sufficient enough to induce reactive oxygen species (ROS) generation. Surprisingly, there were no significant (p > 0.05) changes in FRs in the E group as compared with the C group, which indicates that CCV counteracted the effects induced by ROS. BAP increased significantly (p < 0.05) in the E group as compared with the NC group, reflecting the activation of some antioxidant enzymes. Linear regression of FRs on BAP was significant (p < 0.05) in both the C and E groups. Based on the results of this study, it can be concluded that the CCV contains biochemical factors that activate antioxidant enzymes, as evident by elevation in the BAP that depresses ROS formation.

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It is clear that environmental heavy metals influence life systems and reproductive system. In the present study histological investigation revealed that cadmium was testicular toxicant in mice. Here we compared the fine-structure of spermatogenesis in two groups of mice (SWR), experimental and control. The experimental group underwent cadmium ingestion at 1 mg/kg daily for 4 weeks. The control group underwent ingestion of distilled water with equal dosages, using the same type of injectors, for 4-weeks. After cadmium exposure period both control and experimental groups were killed and samples of the testes were processed for microscopic examination. Ultra sections were examined and photographed by Transmission Electron Microscope (JEOL- 100SX) at 80KV. Ultrastructure examination revealed, vascular endothelial, interstitial, and sertoli cells damages. Early impairments of germinal cellular differentiation resulted in deformations in all parts of late spermatid. There were dislocation of accrosomal granules, nuclear damage associated with chromatin heterogeneity, detached spermatid from the apical process of sertoli cell, disarrangement of the mitochondria, abnormal oriented tail piece, and abnormal microtubules complex. These ultra morphological abnormalities relate to cell injury and to the resulting physiological abnormality, necrobiosis. Based on the results of this investigation it can be concluded that cadmium ingestion at 1000 microg/kg caused testicular toxicity and abnormalities in early sperm development.

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In the transition from rest to steady-state exercise, O2 uptake from the lungs (VO2) depends on the product of pulmonary blood flow and pulmonary arteriovenous O2 content difference. The kinetics of pulmonary blood flow are believed to be somewhat faster than changes in pulmonary arteriovenous O2 content difference. We hypothesized that during CO breathing, the kinetics of CO uptake (VCO) and diffusing capacity for CO (DLCO) should be faster than VO2 because changes in pulmonary arteriovenous CO content difference should be relatively small. Six subjects went abruptly from rest to constant exercise (inspired CO fraction = 0.0005) at 40, 60, and 80% of their peak VO2, measured with an incremental test (VO2peak). At all exercise levels, DLCO and VCO rose faster than VO2 (P less than 0.001), and DLCO rose faster than VCO (P less than 0.001). For example, at 40% VO2peak, the time constant (tau) for DLCO in phase 2 was 19 +/- 5 (SD), 24 +/- 5 s for VCO, and 33 +/- 5 s for VO2. Both VCO and DLCO increased with exercise intensity but to a lesser degree than VO2 at all exercise intensities (P less than 0.001). In addition, no significant rise in DLCO was observed between 60 and 80% VO2peak. We conclude that the kinetics of VCO and DLCO are faster than VO2, suggesting that VCO and DLCO kinetics reflect, to a greater extent, changes in pulmonary blood flow and thus recruitment of alveolar-capillary surface area. However, other factors, such as the time course of ventilation, may also be involved.(ABSTRACT TRUNCATED AT 250 WORDS)

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To investigate the combined effect of water immersion (WI) and lean body mass on cardiac output (Q), 12 healthy young men, 6 lean (fat less than 9%) and 6 fat (fat greater than 18%), were studied at rest and during steady state exercise approximating 30-40% Vo2 max under three experimental conditions. There were on land at 24 degrees C (LND), and immersed in water at 33-34 degrees C to hip level (HIP), and to the xiphoid (XIP). Metabolic measures were determined during 30-s periods from the average breath measurements. Mixed venous PCO2 (PVCO2) was estimated using rebreathing equilibration technique. Cardiac output was calculated by the indirect Fick's principle. In the lean individuals the average Q rose from a resting value of 5.43 +/- 0.43 (LND) to an exercise value of 7.25 +/- 0.40 L/min (XIP), and from resting value of 5.62 +/- 0.40 to an exercise 6.47 +/- 0.5 L/min in the fat individuals. During exercise, the associated increase in Q with increasing WI was significantly (p less than 0.05) higher compared with the land experiments. Inspection of the mean profile corresponding to this increase indicated that an increase in the level of immersion results in a significant (p less than 0.05) increase in the average Q for the lean group. For the fat group, the average Q was significantly (p less than 0.05) larger only at XIP level. At rest, heart rate dropped from 67 +/- 3.36 (LND) to 60 +/- 4.13 (XIP), and from 79 +/- 3.73 to 73 +/- 4.10 BPM for the lean and fat group, respectively. MANOVA analysis showed a significant (p less than 0.05) interaction between WI and group membership, indicating that the effect of WI is significantly different between the two groups. These data indicate that the change in central blood volume with WI depends, in part, on the lean mass of the body.

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A simple, economic, and accurate microprocessor system for the determination of mixed venous PCO2 has been described. Through the automatic gas mixing system, it is possible to facilitate the use of the rebreathing equilibration technique for the purpose of cardiac output calculations. It was also possible to flush the rebreathing bag within a brief time, providing the investigator with an automatic three-way valve driven by a solenoid.

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The purpose of this study was to compare CO2 storage capacity of endurance and sprint-trained athletes during steady state exercise. Ten subjects, five sprinters and five distance runners, performed a submaximal treadmill exercise at two different work rates, 45% and 65% of VO2max. CO2 storage capacity was determined by measuring the excess CO2 washout associated with hyperventilation, normalized for body weight and expressed per unit change in mixed venous PCO2 (ml kg-1 Torr-1). Mixed venous PCO2 (PvCO2) was measured by rebreathing equilibration. It was found that CO2 storage capacities of the runners were significantly (P less than 0.05) greater than the sprinters at the two work rates. The sprinters CO2 storage capacities were 2.69 and 2.14 ml kg-1 Torr-1 at low and high work rates, respectively. The corresponding mean values for the runners were 4.56 and 3.92 ml kg-1 Torr-1, respectively. These results may be explained by the metabolic differences between the sprinters and runners. The sprinters' musculature depends more heavily on the glycolytic metabolic pathway, which is associated with an increased lactate production and hence a reduction in the combining power of the blood for CO2 during exercise. At the low work rate, the body's storage capacity for CO2 was significantly (P less than 0.05) greater than the higher work rate for both groups. Obviously, at the higher work level more blood would be presented to the lungs per unit time allowing an increase in CO2 clearance from the body stores.

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