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1 e to such damage, caused by an environmental toxicant.
2 ssible impacts on sensitivity estimates to a toxicant.
3 persistent and bioaccumulative environmental toxicant.
4 odes of action of a widespread environmental toxicant.
5 mals, we conclude that BPA is a reproductive toxicant.
6 rtilization (IVF), we consider it an ovarian toxicant.
7 90% using elemental mercury as a model vapor toxicant.
8        Methylmercury (MeHg) is a known neuro-toxicant.
9 endocrine disruptor, is a neurodevelopmental toxicant.
10 hthylisothiocyanate (ANIT), a BDEC-selective toxicant.
11 ice accumulates arsenic, an established lung toxicant.
12 a means of assessing the role of a potential toxicant.
13  species diversity hinders the adaptation to toxicants.
14 regnancy disruptive effects of environmental toxicants.
15 fish communities challenged by anthropogenic toxicants.
16 ong with the susceptibility of each stage to toxicants.
17 icity differences among a variety of similar toxicants.
18  as wood preservatives, and as environmental toxicants.
19      Cyanogenic glycosides are natural plant toxicants.
20 lobacter salinarum that dimerizes to extrude toxicants.
21 responses following exposure to some contact toxicants.
22 lying the cytotoxic effects of environmental toxicants.
23 nd early childhood exposure to environmental toxicants.
24  technique for unmasking negative effects of toxicants.
25 tematic approach for identifying responsible toxicants.
26  a role in cell cycle changes in response to toxicants.
27 also play a role in risks from environmental toxicants.
28 ve lung injury caused by smoke and pulmonary toxicants.
29 city aiding in the identification of primary toxicants.
30 s of chironomid larvae exposed to four model toxicants.
31 ood, are known carcinogens and developmental toxicants.
32 ers that inhibit the release or transport of toxicants.
33 n shown to be reproductive and developmental toxicants.
34 ased mechanistic profiling of potential (eco)toxicants.
35  the physicochemical properties of potential toxicants.
36 sity and fat metabolism in lieu of exogenous toxicants.
37 ures, antibiotic exposure, and environmental toxicants.
38 d as the result of exposure to environmental toxicants.
39 c acids (NAs) are one of the main persistent toxicants.
40 ng from disease or exposure to environmental toxicants.
41 cies or those associated with high levels of toxicants.
42 strongly increase the synergistic effects of toxicants.
43 redictive modeling results suggested 90% are toxicants.
44 onal known and suspected female reproductive toxicants.
45 ks of simultaneous exposure to environmental toxicants.
46 be induced by various diseases and exogenous toxicants.
47  waste and their potency as emerging organic toxicants.
48 n from neurotoxic insult by the dopaminergic toxicant 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (M
49 neuronal cells treated with the parkinsonian toxicant 1-methyl-4-phenylpyridinium (MPP(+)) as well as
50 tered after exposure to the model testicular toxicant, 2,5-hexanedione (HD) using microarrays; 2) exp
51                                Environmental toxicant accumulation is modifiable; public health polic
52                  Studies have shown that the toxicant-activated aryl hydrocarbon receptor (AHR) may d
53 hance our understanding of how environmental toxicants affect brain function.
54                                Environmental toxicants affect human health in various ways.
55 sure is one of the most common environmental toxicants affecting children.
56 d using traditional removal methods, such as toxicants aimed at rodents, these approaches have limita
57 e to either temperature or time with the air toxicant analyte, and various concentrations thereof).
58    Chronic exposure to arsenic (As), a human toxicant and carcinogen, remains a global public health
59 , an in vivo metabolite of the environmental toxicant and common environmental pollutant trichloroeth
60                     Arsenic is an epigenetic toxicant and could influence fetal developmental program
61                      Nitromethane is a known toxicant and suspected human carcinogen.
62    Assessment of exposure to tobacco-related toxicants and carcinogens at the population level is thu
63  protect cells and tissues from a variety of toxicants and carcinogens by increasing the expression o
64  simultaneous measurement of tobacco-related toxicants and carcinogens in wastewater are not availabl
65 insight into the population exposure to both toxicants and carcinogens resulting from tobacco use.
66 ty and carcinogenic potency of a plethora of toxicants and carcinogens.
67 er 344 rats to low doses of model testicular toxicants and classically characterized the testicular i
68 ants, including small volatile environmental toxicants and endogenous algogenic lipids(1).
69         Long-term exposures to environmental toxicants and endogenous electrophiles are causative fac
70 table to ancestral exposure to environmental toxicants and epigenetic transgenerational inheritance m
71 based on a survey of known male reproductive toxicants and established mechanisms and pathways of tox
72 pragmatism in the selection of volatiles and toxicants and in defining their roles in formulations.
73 udied the impacts of smoked cigarette filter toxicants and microfibres on the polychaete worm Hediste
74 the waterpipe, hookah smoke delivers tobacco toxicants and nicotine plus charcoal combustion products
75 ul for the detection of a variety of harmful toxicants and pathogens to protect human health and nati
76 everages and soups are good to cleanse liver toxicants and prevent liver diseases.
77 ity, poor diet, environmental and industrial toxicants and psychological stress.
78                 The actions of environmental toxicants and relevant mixtures in promoting the epigene
79 sed extensively for studies on environmental toxicants and salt (NaCl) homeostasis.
80 uals who worked on the spill were exposed to toxicants and stressors that could lead to adverse effec
81 s developed and applied for the detection of toxicants and/or inhibitors to digesters.
82 dered carcinogenic and/or neurodevelopmental toxicants, and children's exposure to these compounds is
83 ninvasive tool to screen new drugs, evaluate toxicants, and elucidate disease mechanisms.
84 ater column to smoking debris and associated toxicants, and highlight the risks posed by smoked cigar
85  models to distinguish metals from non-metal toxicants, and individual metal from one another, and fu
86  in the food and water supply, environmental toxicants, and infectious agents.
87 exogenous stressors such as heat, infection, toxicants, and ischemia, our results indicate that HSP70
88         Exposure to environmental stressors, toxicants, and nutrient deficiencies can affect DNA in s
89  the most commonly encountered environmental toxicants, and research from model systems has suggested
90  respect to their detection capabilities for toxicants, and therefore offering an interesting perspec
91 nary TFF3 levels did not respond to nonrenal toxicants, and urinary albumin faithfully reflected alte
92 n increase species sensitivities to chemical toxicants, and vice versa, and the recent insight that t
93  which in utero adjustments to environmental toxicants are conferred.
94 known as an effective mutagen, clastogen and toxicant as well as an effective inducer of sister-chrom
95 e as potent Ahr activators and developmental toxicants as PAHs.
96  generally applicable to other environmental toxicants as well as pharmaceutical drugs.
97 he detection of low molecular weight natural toxicants, as an alternative to toxin-conjugates.
98  Inorganic arsenic (iAs) is an environmental toxicant associated with an increased risk of prostate c
99 relation to exposure to common environmental toxicants at current levels.
100 e-cell array system for a diverse variety of toxicants at different dose concentrations.
101 nsumers reduce exposure to mercury and other toxicants at the cost of reduction in cardioprotective f
102 rong evidence suggests that BPA is a uterine toxicant because it impaired uterine endometrial prolife
103 rstanding kinetic and geochemical effects on toxicant bioavailability is key, and these are influence
104               Peroxynitrite is an endogenous toxicant but is also a cytotoxic effector against invadi
105 ches was less than 5-fold, covering baseline toxicants but as well compounds with presumed specific m
106 docrine disruptor and potential reproductive toxicant, but results of epidemiologic studies have been
107 bstances (PFASs) are suspected developmental toxicants, but data on PFAS concentrations and exposure
108 ine pesticides (OCPs) are neurodevelopmental toxicants, but few studies have examined associations wi
109  organic pollutants (POPs) are developmental toxicants, but the impact of both maternal and paternal
110 ), mercury (Hg), and cadmium (Cd), are known toxicants, but their associations with the thyroid axis
111                Exposure to the environmental toxicant cadmium (Cd) contributes to the development of
112  how early-life exposure to an environmental toxicant can be a risk factor for childhood obesity.
113  suggest that exposure to the same amount of toxicants can disproportionately compromise ecosystem pr
114           Although defining the effects that toxicants can have on the immune system is a valuable co
115 s after exposure to another model testicular toxicant, carbendazim (CBZ).
116 thermore use this information for successful toxicant classification in unknown samples.
117                     Small-molecule drugs and toxicants commonly interact with more than a single prot
118 es that were exposed to substantially higher toxicant concentrations after the sixth generation were
119                                              Toxicant concentrations were highest and had the greates
120 ential mechanism through which environmental toxicants contribute to PD pathogenesis.
121 ity guideline values (GVs) for two reference toxicants, copper and the herbicide diuron, for tropical
122 tinuous microfluidic perfusion as a means of toxicant delivery.
123  (PAHs) are widely distributed environmental toxicants derived from sources that include cigarette sm
124 amaging effects of exposure to environmental toxicants differentially affect genetically distinct ind
125   Although results infer that sensitivity to toxicants differs across biogeographic ranges, shallow-w
126 toxicology for years as the receptor for the toxicant dioxin, is rapidly gaining interest in immunolo
127 tous compound that is emerging as a possible toxicant during embryonic development.
128 n change following exposure to environmental toxicants, e.g., heavy metals.
129 re of social insect colonies to distribute a toxicant effectively within the colony.
130 rence increased our process understanding of toxicant effects in macroinvertebrate communities and he
131                                              Toxicant effects on feeding and maintenance resulted in
132 ly Life Exposures in Mexico to Environmental Toxicants (ELEMENT) project.
133 can be adapted to accommodate other types of toxicant, environmental samples and other aquatic ovipar
134 ted rat liver shows striking similarity with toxicant-exposed cells in vivo, indicating that gross sy
135 e Chironomus riparius to withstand long-term toxicant exposure has been attributed to genetic adaptat
136 This study examined the genetic mutation and toxicant exposure in producing gut microbiota alteration
137 ed that gene expression is more sensitive to toxicant exposure than life cycle end points, underlinin
138 ius can indeed withstand long-term sublethal toxicant exposure through phenotypic plasticity without
139 ronomus riparius indeed copes with prolonged toxicant exposure through phenotypic plasticity.
140 luency, they were used for studies including toxicant exposure, immunoblotting, immunofluorescence an
141 pressed proteins in small fish species after toxicant exposure.
142 s, higher fish intake often leads to greater toxicant exposure.
143 ls in more susceptible stages at the time of toxicant exposure.
144 tory of a single organism and the effects of toxicant exposure.
145 ous, and pregnancy is a sensitive window for toxicant exposure.
146  mitochondrial dysfunction and environmental toxicant exposures ('four major areas').
147 ochondrial dysfunction (145 of 153, 95%) and toxicant exposures (170 of 190, 89%).
148 flammation and oxidative stress, followed by toxicant exposures and mitochondrial dysfunction.
149 he relevance of preconceptional and prenatal toxicant exposures for genomic stability in offspring is
150 ace, little is known about the potential for toxicant exposures in a parental (F0) generation to affe
151 s best known for responding to environmental toxicant exposures to induce a battery of xenobiotic-met
152 ysregulation/inflammation, oxidative stress, toxicant exposures, genetics and neuroimaging.
153  between miRNA and mRNA due to environmental toxicant exposures.
154  which may alter human risks associated with toxicant exposures.
155 rating and differentiated cell mitochondrial toxicant exposures.
156  However, mapping only adverse outcomes of a toxicant falls short of describing the stress or adaptiv
157 en redesigned to help identify environmental toxicants, food contaminants and supplements, drugs, and
158 ed in this study not only can quickly detect toxicants for anaerobic digestion but also can efficient
159 c (iAs/As(2) O(3) (2-) ) is an environmental toxicant found in watersheds around the world including
160 stolochic acids I and II are prevalent plant toxicants found in the Aristolochiaceae plant family.
161 ty in chemicals and potentially prevent some toxicants from entering common use.
162 the offspring generations (F1-F5), after the toxicant had been removed from the diet.
163                  Warming in combination with toxicants had little effect at the individual and popula
164 nvestigating combined effects of warming and toxicants has been a topic of little research, but negle
165 earch on neurodevelopmental effects of these toxicants has produced conflicting results.
166  It is recognized that cellular responses to toxicants have a highly dynamic nature, and exhibit both
167 mental exposures to a variety of factors and toxicants have been shown to promote the epigenetic tran
168                                        These toxicants have detrimental effects on the human body and
169  humans exposed to famine, stress/trauma, or toxicants have provided evidence that parental exposure
170 tigations of ENMs (as opposed to traditional toxicants) have been reported, but have not yet been sys
171      A number of environmental factors (e.g. toxicants) have been shown to promote the epigenetic tra
172 hazard identification to female reproductive toxicant hazard identification.
173  of contamination by methylmercury and other toxicants, higher fish intake often leads to greater tox
174 effect on behavior, fitness, and response to toxicants; however, this is rarely considered in ecotoxi
175 LB/cJ mice were exposed to different contact toxicants, identifying trimellitic anhydride (TMA) for f
176 es also suggest that BPA may be a testicular toxicant in animal models, but the data in humans are eq
177 ce nutrient and, at higher concentrations, a toxicant in natural waters, with the relative rates of t
178             Selenium (Se) is a developmental toxicant in oviparous vertebrates.
179  larger role of melamine as an environmental toxicant in producing the pathology in similar cellular
180 Acetaminophen (APAP) is a proven lethal oral toxicant in reptiles but the physiological mechanism is
181 s is crucial to predict the future impact of toxicants in a warming world.
182  ethoxylates (NP(EO)n and OP(EO)n) are major toxicants in agrochemicals used around beehives.
183                                 Detection of toxicants in bronchoalveolar-lavage (BAL) fluid from pat
184 ed with tumorigenic potency of environmental toxicants in coexposure scenarios, including possible sy
185 analysis (EDA) enables the identification of toxicants in complex contaminated environmental samples.
186 omplex environmental mixtures to responsible toxicants in effect-directed analysis (EDA).
187 t also has the ability to degrade halophenol toxicants in its living environment.
188 ts (DBPs) are reproductive and developmental toxicants in laboratory animals.
189 ate, transport, and bioavailability of these toxicants in organisms.
190  studies also show the role of environmental toxicants in perturbing the gut microbiome and its metab
191  Ragworms exposed to smoked cigarette filter toxicants in seawater at concentrations 60 fold lower th
192 Therefore, when organisms are exposed to two toxicants in sequence, the toxicity can differ if their
193 tured nanoparticles (NPs) can associate with toxicants in the aqueous phase and these associations ca
194 al clusters into an ensemble model, chemical toxicants in the external test set were evaluated for pu
195 tes makes it important to be able to monitor toxicants in the feed to anaerobic digesters to optimize
196 isms that facilitate or hinder adaptation to toxicants in the field.
197   Molecular dynamics simulations of these 14 toxicants in the pore region of the alpha1beta2gamma2 GA
198 igenetic effects of individual environmental toxicants in tobacco remain largely unexplored.
199 aceuticals were confirmed to act as baseline toxicants in zebrafish.
200 olychlorinated biphenyls (PCBs) were used as toxicant, in concentrations of 0.02 mug/ml, 0.04 mug/ml,
201 nd a novel susceptibility factor to drug- or toxicant-induced acute liver injuries.
202 aspermatogenesis reboots meiosis and reseals toxicant-induced BTB disruption, even though it fails to
203 xplore the molecular mechanism(s) underlying toxicant-induced cell injury.
204                         We hypothesized that toxicant-induced testicular injury can be detected in sp
205  mRNA transcripts are indicators of low dose toxicant-induced testicular injury in the rat.
206 nce that arsenic, a widespread environmental toxicant, inhibits erythropoiesis likely through replaci
207                                      Vapers' toxicant intake was calculated for scenarios in which di
208        Identification of female reproductive toxicants is currently based largely on integrated epide
209 xposure to nerve agents and organophosphorus toxicants is due to irreversible inhibition of acetylcho
210 nd early childhood exposure to environmental toxicants is increasingly recognized as contributing to
211                           The disposition of toxicants is often affected by their binding to serum pr
212  the various assays used to screen potential toxicants is the antioxidant response element beta lacta
213 iption factor that responds to environmental toxicants, is increasingly recognized as a key player in
214 y only when, in the absence of exposure to a toxicant, it has a parasitic interaction with the host p
215 odibenzo-p-dioxin (TCDD) is an environmental toxicant known to inhibit Ab secretion and Ig expression
216                  Air pollution contains many toxicants known to affect neurological function and to h
217 model to examine the dependence of offspring toxicant load on birth order, food density, and interspe
218 or hydrolyzing various xenobiotic agents and toxicants, many of which target the central and peripher
219 ted the hypothesis that common environmental toxicants may also impair cholesterol metabolism and the
220 igate how prenatal exposure to environmental toxicants may alter the typical developmental trajectory
221 omplex I, either by mutations or exposure to toxicants, may be a risk factor for Parkinson's disease.
222                                              Toxicant measures were linked to pod, age, and birth ord
223 s and reseals blood-testis barrier following toxicant-mediated aspermatogenesis and barrier disruptio
224 ated with various dose levels of three model toxicants, mitomycin C, hydrogen peroxide, and lead nitr
225  constraint on adaptive solutions to complex toxicant mixtures at each site.
226 res on EED development, including a role for toxicant modulation of gut immune system and microbiome
227 ough scat employed in this study may improve toxicant monitoring in the marine environment and promot
228 antageous in the study where further organic toxicants occurred.
229                            Mercury (Hg) is a toxicant of global concern that accumulates in organisms
230 s and exposure pathways, identify additional toxicants of concern and populations at risk, and examin
231 ted here can be broadly applied because many toxicants of different chemical classes are electrophile
232 d reliably describes the effects of chemical toxicants on C. elegans growth and development.
233       While studies of the direct effects of toxicants on exposed organisms are commonplace, little i
234 1-+4 degrees C), the effects of hypothetical toxicants on suborganismal processes, including feeding,
235 d as pesticides, mycotoxins, process-induced toxicants or packaging contaminants, were carefully chos
236 s such as the possibility that environmental toxicants or viruses may initiate PD pathogenesis in the
237  and helps flush mucus and inhaled pathogens/toxicants out of the lung.
238           Our aim is to show conservation of toxicant pathways and cellular targets across vertebrate
239 lorinated biphenyls (PCBs) are environmental toxicants; PCB exposure has been associated with adverse
240 anged from tens to thousands of nanograms of toxicants per milligram of e-liquid vaporized, and they
241 ral similarities to the highly characterized toxicants polychlorinated dibenzo-p-dioxins.
242                            Inhaled oxidative toxicants present in ambient air cause airway epithelial
243  associated with AalphaC and other arylamine toxicants present in tobacco smoke.
244 responses globally upon exposure to chemical toxicants, presents promises for next-generation toxicit
245 ity of E. verrucosus to persisting low-level toxicant pressure.
246                           The two testicular toxicants produced distinct molecular signatures with on
247                                    The liver toxicants profile contained the ARE-bla and relevant Pub
248                    We conclude that repeated toxicant pulse of populations that are challenged with i
249                                      Contact toxicant reactions are accompanied by localized skin inf
250 nophil-mediated events following TMA contact toxicant reactions increase skin sensory nerve substance
251                                     Adaptive toxicant resistance has rapidly evolved in Gulf killifis
252 tion and, thus, the potential for developing toxicant resistance.
253 (PAHs), the widely distributed environmental toxicants shown to induce porphyrin accumulation causing
254    This is illustrated by the observation of toxicant-specific changes in the spectrum of tRNA modifi
255                                 However, the toxicants stored in lipids may have more substantial imp
256 s affect exposure dose and the nature of the toxicant studied and have a direct impact on all (eco)to
257 ly Life Exposures in Mexico to Environmental Toxicants) study during 1994-1995.
258 ll cycle creating a significant concern that toxicants such as ddC impair mtDNA maintenance in both p
259                                Environmental toxicants such as industrial wastes, air particulates fr
260                  With this method, different toxicants such as metals and organic compounds were anal
261                                              Toxicants such as organochlorine insecticides, lead ammu
262                                Environmental toxicants such as pesticides exert strong selection pres
263                    Exposure to environmental toxicants, such as inorganic arsenic (iAs), has also bee
264  is known about whether prenatal exposure to toxicants, such as lead, may also confer such risks.
265                               The effects of toxicants, such as pesticides, may be more severe for so
266 include diverse compounds from environmental toxicants, such as TCDD, that are carcinogenic to dietar
267  (Cd) is a naturally occurring environmental toxicant that disrupts mitochondrial function at occupat
268 n of tolerance to hydrogen sulfide (H(2)S)-a toxicant that impairs mitochondrial function-across evol
269 reshwater crustacean Gammarus pulex and four toxicants that act on different targets (diazinon, propi
270 istant coatings, are suspected developmental toxicants that are ubiquitous and persistent in the envi
271  common worldwide and produces environmental toxicants that may influence health; however, biologic e
272 Arsenic and cadmium are known cardiovascular toxicants that pose disproportionate risk to rural commu
273 or the readout of the biological effect of a toxicant through metabolomic-derived pathway analysis, a
274 posed to relatively enriched levels of metal toxicants through their habitat and lifestyle, and this
275 nteractions in ant colonies to disseminate a toxicant throughout the colony.
276 rigins that can contaminate water and become toxicants to aquatic species or other living beings via
277  microfibres (cellulose acetate) and harmful toxicants to marine environments.
278 ation into the contribution of environmental toxicants to the risk of preeclampsia has been sparse.
279     This study emphasizes the need to assess toxicants together with other risk factors relevant to h
280 understanding of an organism's response to a toxicant under ecologically relevant conditions and prov
281 rmal evolution to improve risk assessment of toxicants under global warming.
282 osure order in ecological risk assessment of toxicants under realistic combinations with natural stre
283 environmental pollutants may be reproductive toxicants underscores the need for prospective studies o
284                Our study suggests that metal toxicant uptake and essential element deficiency during
285 rooctanesulfonate (PFOS) is an environmental toxicant used in developing countries, including China,
286 rray, able to detect four different types of toxicants, using a single photodetector (photomultiplier
287 ass spectrometry to measure several priority toxicants: vitamin E acetate, plant oils, medium-chain t
288 ght key characteristics of male reproductive toxicants was based on a survey of known male reproducti
289                   Human BChE inhibited by OP toxicants was incubated for 4 days to 6 years.
290 rent toxicity when the exposure order of two toxicants was reversed, while maintaining the same dose.
291 disease status and exposure to environmental toxicants, we sought to develop a rapid, sensitive, and
292        Potential toxicophores for well-known toxicants were created by identifying chemical features
293                            No other priority toxicants were found in BAL fluid from the case patients
294                           In addition, these toxicants were likely from endogenous lipid stores.
295                                        Liver toxicants were used as probe compounds to search PubChem
296 al oxidative stress response for known liver toxicants when no ARE-bla data were available.
297 ny insecticides are bird, fish, and honeybee toxicants, whereas herbicides and fungicides pose fewer
298 re able to distinguish metals from non-metal toxicants with 100% accuracy.
299 for the frequently occurring combinations of toxicants with natural stressors.
300  an exogenous role as a receptor for manmade toxicants, with their binding leading to transcription o

 
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