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Toxicology of Air Pollution
Published in Lorris G. Cockerham, Barbara S. Shane, Basic Environmental Toxicology, 2019
Donald E. Gardner, Susan C. M. Gardner
Toxicity Profile. The toxicity of lead is due to its ability to bind to biologically important molecules, disrupting physiological functions. Hematological, neurological, and renal effects have been associated with lead toxicity at low lead exposures. Lead toxicity is due in part to depletion of heme because of the direct inhibition of delta-aminolevulinic acid dehydratase and other enzymes involved in heme biosynthesis (Dresner et al., 1982). The resulting anemia is due to a shortening of erythrocyte survival time. Neurological effects have been demonstrated at blood lead levels as low as 40 to 60 µg/dl in adults and may be responsible for altered behavior and decreases in IQ (Lilis et al., 1977; Irwig et al., 1978; Hammond et al., 1980). Morphological changes in renal mitochondria are an early response to lead exposure (Goyer and Rhyne, 1973). Lead induced nephropathy has been seen in humans at blood levels between 40 and 100 µg/dl. Reproductive and developmental processes can also be adversely affected by lead exposures (Lane, 1949). Lead is readily transferred across the placenta and in rodent studies fetotoxicity has occurred at a concentration of 10 µg/m3 (U.S. EPA, 1986). Epidemiologic studies indicate that fetal exposure to lead may have undesirable effects on mental development of the newborn and the length of the gestation period. In the male, lead may have an adverse effect on the development of sperm and the seminal vesicles.
Hazards assessment of the intake of trace metals by common mallow (Malva parviflora K.) growing in polluted soils
Published in International Journal of Phytoremediation, 2019
Tarek M. Galal, Zeinab A. Shedeed, Loutfy M. Hassan
In addition, Appenroth (2010) reported the adverse effects of trace/heavy metals on the light and dark reactions of photosynthesis as well as on the reduction of chlorophyl content, stomatal conductance, and transpiration rates. Moreover, several mechanisms have been proposed for metals-induced decrease in pigment contents, which include distorted chloroplast ultra-structure, decrease in the activities of delta- aminolevulinic acid dehydratase and ferredoxin NADP + reductase, inhibition of plastoquinone and carotenoid synthesis, hindrance in electron transport chain, and Calvin cycle inhibition (Pourrut et al.2013). These mechanisms include: (a) some elements (as Pb) reduce the uptake of chlorophyl-essential elements such as Mg and Fe; (b) decreasing rate of photosynthetic pigment accumulation (with Pb treatment) may be the consequence of peroxidation of chloroplast membranes due to increased level of ROS generation (Malar et al.2014); and (c) the concomitant pheophytin accumulation and oxidative stress have been observed in plants exposed to toxic concentrations of elements (Mobin and Khan 2007; Gomes et al.2016). This is because, under stress conditions, part of chlorophylls might be converted to pheophytins (Pheophytins are compounds formed during the chlorophyl degradation [Sanmartin et al.2011]).
Lead induces DNA damage and alteration of ALAD and antioxidant genes mRNA expression in construction site workers
Published in Archives of Environmental & Occupational Health, 2019
Zertashia Akram, Sadaf Riaz, Mahmood Akhtar Kayani, Sarwat Jahan, Malik Waqar Ahmad, Muhammad Abaid Ullah, Hizbullah Wazir, Ishrat Mahjabeen
Additionally, lead inhibits three enzymes in the heme biosynthesis pathway: delta-aminolevulinic acid dehydratase (ALAD), coporphyrinogen oxidase, and ferrochelatase. But its effects on ALAD are the most profound.14 Exposure to lead may also result in significant adverse health effects to hepatic and renal systems.15–17 Lead strongly inhibits ALAD enzyme stoichiometrically, changes the enzyme's quaternary structure, and initiated the lead-induced toxicity in brain, renal region, and in reproductive organs.18,19 Many earlier studies have reported the association of ALAD polymorphisms with lead-induced toxicity in different body organs, such as hepatic region, renal region, brain region, and different reproductive organs.20–22 To date, no study is available for expression variations of ALAD gene in lead-exposed individuals in Pakistani population.
Biomarkers of exposure and effect in a working population exposed to lead, manganese and arsenic
Published in Journal of Toxicology and Environmental Health, Part A, 2018
Daniela C Serrazina, Vanda Lopes De Andrade, Madalena Cota, Maria Luísa Mateus, Michael Aschner, Ana Paula Marreilha dos Santos
With evidence of cholinergic and heme synthesis alterations induced by Pb, Mn and As, several potential effect BMs were considered. Ademuyiwa et al. (2007) suggested that acetylcholinesterase (AChE) activity in erythrocytes might serve as a peripheral surrogate dose-effect index of neurotoxicity in cholinergic function in Pb occupationally exposed individuals. Miners exposed chronically to exceedingly high levels of Mn exhibit altered blood AChE activity and acetylcholine levels (Finkelstein, Milatovic, and Aschner 2007). Red blood cells-AChE activity was also changed in miners and other occupational types of exposed workers (Finkelstein, Milatovic, and Aschner 2007). Both arsenite and arsenate forms induce cholinergic dysfunctions in rats in a dose-dependent manner with concomitant AChE inhibition (Devi, Kumari, and Indravathi 2014; Rodríguez, Jiménez-Capdeville, and Giordano 2003). Lead-mediated effects on heme synthesis are well-(ATSDR 2007a; Goering and Fowler 1987; Seth et al. 1976), resulting in altered heme biosynthesis in the same way as seen in inherited porphyrias (Moore 1998). To date, delta-aminolevulinic acid (ALA, a heme precursor) in urine and delta-aminolevulinic acid dehydratase activity in blood are considered reliable indicators of Pb intoxication (Chiba et al. 1996; Reckziegel et al. 2011; Rocha et al. 1995; Sakai 2000). With respect to Mn-induced hematological effects, only few and inconsistent results exist (Maines 1980). In addition, the range of effects that As produces on enzymes responsible for heme biosynthesis are among the most promising BMs and hence, the porphyrins profile is a useful indicator for biological effect of As exposure (Wu et al. 2004).