PubMed HealthSearch

PubMed · 4189813

Lead effects on corn mitochondrial respiration.

Abstract

Oxidation of exogenous nicotinamide-adenine dinucleotide and succinate by corn mitochondria was measured as a function of lead chloride concentration. Lead chloride (50 to 62 micromoles per liter) stimulated oxidation of exogenous reduced nicotinamide-adenine dinucleotide by 174 to 640 percent depending on the reaction mediums, whereas lead chloride (12.5 micromoles per liter) inhibited succinate oxidation by more than 80 percent. When inorganic phosphate was included in reaction mediums the subsequent addition of lead was without effect due to the low solubility of lead phosphate. If addition of lead was followed by addition of phosphate the inhibition of succinate oxidation by lead was released, but there was no reduction in the stimulation of oxidation of reduced nicotinamide-adenine dinucleotide by lead. The effects of lead on plant growth might be accentuated under conditions of phosphate deficiency.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

D E Koeppe, R J Miller. 1970-03-06. Lead effects on corn mitochondrial respiration.. https://doi.org/10.1126/science.167.3923.1376

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

An integrated multiscale air quality modelling framework for industrial park pollution: Linking local emissions to regional transport.

Capturing the spatiotemporal distribution of pollutants in industrial parks remains challenging for regional air quality models because of their coarse resolution (3 km), resulting in uncertainties in local emission quantification. To address this, we developed the Integrated Multiscale Air Quality Modelling System for Industry (IAQMS-Industry), coupling the regional Nested Air Quality Prediction Modelling System (NAQPMS) with a city-scale chemical transport model. This framework integrates point-source locations and Gaussian plume dispersion to simulate particulate matter with a diameter smaller than 2.5 micrometres (PM2.5) at 100 m resolution. Applied to the Beijing Yi Zhuang and Tangshan industrial parks and evaluated against observations. The coupled model achieved a normalized mean bias (NMB) ranging from 3.1 % to 6.2 %, improving upon NAQPMS (-16.9 % to -7.7 %). Spatial analysis revealed that coarse regional grids underestimated the PM2.5​ concentrations at industrial sites by smoothing gradients, whereas IAQMS-Industry successfully resolved spatial patterns. Industrial point emissions accounted for 22.9 %-26.4 % of PM2.5 in the coupled model, which was significantly greater than the regional model estimates of 1.6 %-13.7 %. These findings indicate that regional models overestimate pollutant dispersion processes in industrial parks while underestimating local industrial impacts. By explicitly resolving point-source dynamics and linking them to regional transport, IAQMS-Industry provides a robust tool for designing targeted emission controls in industrial cities and balancing local air quality improvements with minimized regional pollution outflow. This study underscores the necessity of multiscale modelling for accurate source apportionment and informed environmental governance in industrial zones.

Air Pollution

DNA damage in humans exposed to environmental and dietary polycyclic aromatic hydrocarbons.

The paper describes recent research on human DNA damage related to environmental and dietary polycyclic aromatic hydrocarbon (PAH) exposures. The study populations either represent general populations of large geographical regions, or their exposure situation may have relevance to the general population. In Silesia, Poland, and Northern Bohemia, Czech Republic, where coal-based industry and domestic heating are the major sources of PAHs, significant differences have been observed in white blood cell DNA adducts and cytogenetic biomarkers between environmentally exposed and rural control populations, and significant seasonal variations of DNA damage have been detected. Bus drivers, traffic policemen and local residents have been involved in biomarker studies in Copenhagen, Athens, Genoa and Cairo, and differences have been measured in the level of DNA damage of urban and rural populations. Burning of smoky coal in unvented homes in Xuan Wei region, China, causes high PAH exposure of residents, which has been reflected in DNA adduct levels in different tissues. Indoor wood burning in open fireplaces did not increase human DNA adduct levels. Oil-well fires left burning in Kuwait after the Persian Gulf war created an unprecedented environmental pollution. However, insignificant environmental PAH levels were measured several miles from these fires. Aromatic and PAH-DNA adduct levels in white blood cells of US Army soldiers were lower during their deployment in Kuwait, than in Fulda, Germany, where they were stationed before and after serving in Kuwait. The contribution of dietary PAH exposure to blood cell DNA adduct levels had been demonstrated in studies in which volunteers consumed heavily charbroiled beef. Environmental tobacco smoke did not cause detectable changes, as measured by 32P-postlabelling, in DNA adduct levels in non-smokers. In the reviewed studies, observed DNA adduct levels were generally in the range of 1 to 10 adducts, and not higher than 40 adducts in 108 nucleotides. Typically, 1.5 to 3-fold differences have been detected in DNA adduct levels between the exposed and control groups.

Air Pollution