?-adrenergic receptor density and adenylate cyclase activity in lead-exposed rat brain after cessation of lead exposure

Chang, Huoy-Rou; Tsao, Der-An; Yu, Hsin‐Su; Ho, Chi-Kung

doi:10.1007/s00204-004-0605-9

Cited by 6 publications

(6 citation statements)

References 24 publications

(23 reference statements)

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“…Previous reports indicated that intracellular cAMP and [Ca 2+ ] i are critically involved in lead-mediated signaling pathways and are significantly decreased by lead treatments in rat brain (Ferguson et al 2000;Chang et al 2005). Herein, we found that lead-induced inhibition of human sperm functions are also mediated by intracellular cAMP and [Ca 2+ ] i .…”

Section: Discussionsupporting

confidence: 52%

“…Taken together, these results suggest that the lead-induced decreases in cAMP and [Ca 2+ ] i are common ways of regulating cell functions. It is reported that lead decreased intracellular cAMP by inhibiting the activity of adenylate cyclase (AC), which is the key enzyme involved in synthesizing cAMP (Rodrigues et al 1999;Chang et al 2005). Despite AC is also found in human spermatozoa and involved in regulation of human sperm function (De Jonge et al 1991), Although AC is also found in human spermatozoa and is involved in regulating sperm function, whether it participates in the lead-caused cAMP decreasing requires further study.…”

Section: Discussionmentioning

confidence: 99%

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Lead Inhibits Human Sperm Functions by Reducing the Levels of Intracellular Calcium, cAMP, and Tyrosine Phosphorylation

Zou

Chen

et al. 2016

Tohoku J. Exp. Med.

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It is well known that there has been a worldwide decrease in human male fertility in recent years. One of the main factors affecting this is environmental pollution. Lead is one of the major heavy metal contaminants that threaten the health of animals and human beings in China. It preferentially accumulates in male reproductive organs and can be up to 10 µM in human seminal plasma. Lead impairs mammalian spermatogenesis and sperm quality in vivo. It also inhibits sperm functions in vitro but the underlying mechanisms remain unclear. Therefore, we aimed to investigate the in vitro toxicity of lead on human sperm functions and to elucidate the underlying mechanisms. Semen samples were collected from 20 healthy volunteers with different careers and backgrounds living in Nanchang, Jiangxi. Human sperm suspensions were treated with different concentrations of lead acetate (0, 0.5, 2.5, 10, 50, and 100 µM) and the viability, motility, capacitation and progesterone-induced acrosome reaction were examined. Treatment with 10-100 µ M lead acetate dose-dependently inhibited total and progressive motility measures, capacitation and progesterone-induced acrosome reaction. It also dose-dependently decreased the intracellular concentrations of cyclic adenosine monophosphate (cAMP) and calcium ([Ca 2+ ] i ), and reduced the tyrosine phosphorylation of sperm proteins, all of which are thought to be key factors in the regulation of sperm function. Our findings suggest that lead inhibits human sperm functions by reducing the levels of sperm intracellular cAMP, [Ca 2+ ] i and tyrosine phosphorylation of sperm proteins in vitro.

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Section: Discussionsupporting

confidence: 52%

Section: Discussionmentioning

confidence: 99%

Lead Inhibits Human Sperm Functions by Reducing the Levels of Intracellular Calcium, cAMP, and Tyrosine Phosphorylation

Zou

Chen

et al. 2016

Tohoku J. Exp. Med.

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“…20 -22 Other biologically plausible mechanisms by which lead may increase cardiovascular risk include effects on neuromuscular control of vascular tone and/or central nervous system neurohumoral regulation of vascular function, sodium transport abnormalities, and alterations in cytosolic calcium regulation. [23][24][25][26] Additional research is needed to establish the mechanism responsible for lead-related mortality below 0.48 mol/L(10 g/dL).…”

Section: Discussionmentioning

confidence: 99%

Blood Lead Below 0.48 μmol/L (10 μg/dL) and Mortality Among US Adults

et al. 2006

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Background-Blood lead levels above 0.48 mol/L (10 g/dL) in adults have been associated with increased risk of cardiovascular, cancer, and all-cause mortality. The objective of the present study was to determine the association between blood lead levels below 0.48 mol/L and mortality in the general US population. Methods and Results-Blood lead levels were measured in a nationally representative sample of 13 946 adult participants of the Third National Health and Nutrition Examination Survey recruited in 1988 to 1994 and followed up for up to 12 years for all-cause and cause-specific mortality. The geometric mean blood lead level in study participants was 0.12 mol/L (2.58 g/dL). After multivariate adjustment, the hazard ratios (95% CI) for comparisons of participants in the highest tertile of blood lead (Ն0.17 mol/L [Ն3.62 g/dL]) with those in the lowest tertile (Ͻ0.09 mol/L [Ͻ1.94 g/dL]) were 1.25 (1.04 to 1.51; P trend across tertilesϭ0.002) for all-cause mortality and 1.55 (1.08 to 2.24; P trend across tertilesϭ0.003) for cardiovascular mortality. Blood lead level was significantly associated with both myocardial infarction and stroke mortality, and the association was evident at levels Ͼ0.10 mol/L (Ն2 g/dL). There was no association between blood lead and cancer mortality in this range of exposure. Conclusions-The association between blood lead levels and increased all-cause and cardiovascular mortality was observed at substantially lower blood lead levels than previously reported. Despite the marked decrease in blood lead levels over the past 3 decades, environmental lead exposures remain a significant determinant of cardiovascular mortality in the general population, constituting a major public health problem.

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“…A detailed description of the potential mechanism of neurotoxicity is beyond the scope of this study. Experimental studies in animals suggested as potential mechanisms: stimulation of the sympathetic preganglionic neurons,10 harm to the β-adrenergic system in the brain,11 downregulation of cardiac β1-adrenoceptor activity,14 upregulated expression of P2X4 receptor in satellite glial cells of the stellate ganglion,15 increased sensitivity of chemoreceptor reflex12 or decreased sensitivity of the baroreflex 13. To what extent these animal experiments can be translated to the human condition remains unclear.…”

Section: Discussionmentioning

confidence: 99%

Heart rate variability and peripheral nerve conduction velocity in relation to blood lead in newly hired lead workers

Wei

Yang

et al. 2019

Occup Environ Med

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ObjectivesPrevious studies relating nervous activity to blood lead (BL) levels have limited relevance, because over time environmental and occupational exposure substantially dropped. We investigated the association of heart rate variability (HRV) and median nerve conduction velocity (NCV) with BL using the baseline measurements collected in the Study for Promotion of Health in Recycling Lead (NCT02243904).MethodsIn 328 newly hired men (mean age 28.3 years; participation rate 82.7%), we derived HRV measures (power expressed in normalised units (nu) in the high-frequency (HF) and low-frequency (LF) domains, and LF/HF) prior to long-term occupational lead exposure. Five-minute ECG recordings, obtained in the supine and standing positions, were analysed by Fourier transform or autoregressive modelling, using Cardiax software. Motor NCV was measured at the median nerve by a handheld device (Brevio Nerve Conduction Monitoring System, NeuMed, West Trenton, NJ, USA). BL was determined by inductively coupled plasma mass spectrometry.ResultsMean BL was 4.54 µg/dL (IQR 2.60–8.90 µg/dL). Mean supine and standing values of LF, HF and LF/HF were 50.5 and 21.1 nu and 2.63, and 59.7 and 10.9 nu and 6.31, respectively. Orthostatic stress decreased HF and increased LF (p<0.001). NCV averaged 3.74 m/s. Analyses across thirds of the BL distribution and multivariable-adjusted regression analyses failed to demonstrate any association of HRV or NCV with BL.ConclusionsAt the exposure levels observed in our study, autonomous nervous activity and NCV were not associated with BL.Trial registration numberNCT02243904

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?-adrenergic receptor density and adenylate cyclase activity in lead-exposed rat brain after cessation of lead exposure

Cited by 6 publications

References 24 publications

Lead Inhibits Human Sperm Functions by Reducing the Levels of Intracellular Calcium, cAMP, and Tyrosine Phosphorylation

Lead Inhibits Human Sperm Functions by Reducing the Levels of Intracellular Calcium, cAMP, and Tyrosine Phosphorylation

Blood Lead Below 0.48 μmol/L (10 μg/dL) and Mortality Among US Adults

Heart rate variability and peripheral nerve conduction velocity in relation to blood lead in newly hired lead workers

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