Relevant bibliographies by topics / Cadmium effects on SOD1

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Academic literature on the topic 'Cadmium effects on SOD1'

Author: Grafiati
Published: 10 March 2023

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Journal articles on the topic "Cadmium effects on SOD1"

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Zoidis, Evangelos, George Papadomichelakis, Athanasios C. Pappas, Georgios Theodorou, and Kostas Fegeros. "Effects of Selenium and Cadmium on Breast Muscle Fatty-Acid Composition and Gene Expression of Liver Antioxidant Proteins in Broilers." Antioxidants 8, no. 5 (May 27, 2019): 147. http://dx.doi.org/10.3390/antiox8050147.

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The present work was part of a project intended to evaluate whether organic selenium (Se) has the potential to protect against toxic effects exerted by cadmium (Cd). For this reason, 300 as-hatched, one-day-old broiler chickens were randomly allocated in four dietary treatments with five replicate pens per treatment. Chickens in T1 treatment, were offered a diet supplemented with 0.3 ppm Se (as Se-yeast), without added Cd; in T2 treatment, they were offered a diet with 0.3 ppm Se and 10 ppm Cd; in T3 treatment, they were offered a diet with 0.3 ppm Se and 100 ppm Cd; in T4 treatment, chickens were offered a diet supplemented with 3 ppm Se and 100 ppm Cd. Cadmium was added to the diets in T2, T3, and T4 as CdCl2. On the fourth and sixth weeks, liver and breast samples were obtained from two broilers per replicate pen. Relative gene expression levels of catalase (CAT), superoxide dismutase 1 (SOD1) and 2 (SOD2), methionine sulfoxide reductase A (MSRA) and B3 (MSRB3), iodothyronine deiodinase 1 (DIO1), 2 (DIO2), and 3 (DIO3), glutathione peroxidase 1 (GPX1) and 4 (GPX4), thioredoxin reductase 1 (TXNRD1) and 3 (TXNRD3), and metallothionein 3 (MT3) were analyzed by real-time quantitative PCR in liver, whereas the fatty-acid (FA) profile of breast muscle was determined by gas chromatography. Broilers supplemented with 0.3 ppm Se could tolerate low levels of Cd present in the diets, as there were no significant changes in the breast muscle FA profile, whereas excess Cd led to decreased polyunsaturated fatty acids (PUFAs), and in particular n-6 PUFA. Furthermore, treatments mainly affected the messenger RNA (mRNA) expression of SOD2, TXNRD3, and MT3, while age affected CAT, MSRB3, DIO2, DIO3, GPX4, TXNRD1, and MT3. In conclusion, dietary Se may help against the negative effects of Cd, but cannot be effective when Cd is present at excessive amounts in the diet.
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Bovio, Federica, Barbara Sciandrone, Chiara Urani, Paola Fusi, Matilde Forcella, and Maria Elena Regonesi. "Superoxide dismutase 1 (SOD1) and cadmium: A three models approach to the comprehension of its neurotoxic effects." NeuroToxicology 84 (May 2021): 125–35. http://dx.doi.org/10.1016/j.neuro.2021.03.007.

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Medicherla, Balasubrahmanyam, and Alfred L. Goldberg. "Heat shock and oxygen radicals stimulate ubiquitin-dependent degradation mainly of newly synthesized proteins." Journal of Cell Biology 182, no. 4 (August 25, 2008): 663–73. http://dx.doi.org/10.1083/jcb.200803022.

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Accumulation of misfolded oxidant-damaged proteins is characteristic of many diseases and aging. To understand how cells handle postsynthetically damaged proteins, we studied in Saccharomyces cerevisiae the effects on overall protein degradation of shifting from 30 to 38°C, exposure to reactive oxygen species generators (paraquat or cadmium), or lack of superoxide dismutases. Degradation rates of long-lived proteins (i.e., most cell proteins) were not affected by these insults, even when there was widespread oxidative damage to proteins. However, exposure to 38°C, paraquat, cadmium, or deletion of SOD1 enhanced two- to threefold the degradation of newly synthesized proteins. By 1 h after synthesis, their degradation was not affected by these treatments. Degradation of these damaged cytosolic proteins requires the ubiquitin–proteasome pathway, including the E2s UBC4/UBC5, proteasomal subunit RPN10, and the CDC48–UfD1–NPL4 complex. In yeast lacking these components, the nondegraded polypeptides accumulate as aggregates. Thus, many cytosolic proteins proceed through a prolonged “fragile period” during which they are sensitive to degradation induced by superoxide radicals or increased temperatures.
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Jiang, Shun Yao, and Pei Jiang Zhou. "Effects of Cadmium on the Expression of Antioxidant Enzymes, Oxidative Stress and Apoptosis in Primary Hepatocytes of Carassius Auratus." Advanced Materials Research 518-523 (May 2012): 341–46. http://dx.doi.org/10.4028/www.scientific.net/amr.518-523.341.

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The primary hepatocytes of Carassius auratus were incubated with 0, 0.01, 0.1, 1, 10 and 100 mg/l Cadmium(Cd2+) at 25°C for 8h in vitro. The results showed that the hepatocytes survival rate in the 1, 10 and 100 mg/l Cd2+ treated groups were significantly lower than that in the control, the percentage of apoptotic hepatocytes significantly increased in 0.1, 1 and 10 mg/l of Cd2+ treated groups, intracellular reactive oxygen species(ROS) and malondialdehyde (MDA) content significantly increased in 0.1, 1, 10 and 100 mg/l Cd2+ treated groups, typical DNA ladder was observed in 0.1, 1 and 10 mg/l Cd2+ treated groups, and ruleless DNA fragment occurred in 100 mg/l Cd2+ treated group. The activities of the antioxidant enzymes and the expression of their isozymes activities have similar change tendency, compared with the control group, the activities of superoxide dismutase (SOD) and their isozymes were activated by low concentration of Cd2+ (0.1 and 1 mg/l), however, their activities were inhibited by high concentration of Cd2+ (10 and 100 mg/l), especially, the special isozyme (SOD1) was found in the patterns of SOD isozymes in 0.1 and 1 mg/l Cd2+ treated groups, the activities of peroxidase(POD) and its isozymes significantly reduced with a concentration-dependent manner in all Cd Cd2+ treated groups, the activities of catalase(CAT) and its isozymes significantly decreased in higher concentration Cd2+ treated groups (1, 10 and 100mg/l). The results suggested that Cd2+ could damage the activities of the antioxidant enzymes and cause oxidative stress, lipid peroxidation, DNA fragmentation, apoptosis and necrosis in primary hepatocytes, contributing to the liver toxicity induced by Cd2+.
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Nikolic-Kokic, Aleksandra, Zorana Orescanin-Dusic, Ivan Spasojevic, Dusko Blagojevic, Zorica Stevic, Pavle Andjus, and Mihajlo Spasic. "The effects of wild-type and mutant SOD1 on smooth muscle contraction." Archives of Biological Sciences 67, no. 1 (2015): 187–92. http://dx.doi.org/10.2298/abs141006023n.

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In this work we compared the mutated liver copper zinc-containing superoxide dismutase (SOD1) protein G93A of the transgenic rat model of familial amyotrophic lateral sclerosis (FALS), to wild-type (WT) rat SOD1. We examined their enzymatic activities and effects on isometric contractions of uteri of healthy virgin rats. G93A SOD1 showed a slightly higher activity than WT SOD1 and, in contrast to WT SOD1, G93A SOD1 did not induce smooth muscle relaxation. This result indicates that effects on smooth muscles are not related to SOD1 enzyme activity and suggest that heterodimers of G93A SOD1 form an ion-conducting pore that diminishes the relaxatory effects of SOD1. We propose that this type of pathogenic feedback affects neurons in FALS.
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Sorrells, A. D., K. Corcoran-Gomez, K. A. Eckert, A. G. Fahey, B. L. Hoots, L. B. Charleston, J. S. Charleston, C. R. Roberts, and H. Markowitz. "Effects of environmental enrichment on the amyotrophic lateral sclerosis mouse model." Laboratory Animals 43, no. 2 (April 2009): 182–90. http://dx.doi.org/10.1258/la.2008.005090.

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The manner in which an animal's environment is furnished may have significant implications for animal welfare as well as research outcomes. We evaluated four different housing conditions to determine the effects of what has been considered standard rodent enrichment and the exercise opportunities those environments allow on disease progression in the amyotrophic lateral sclerosis mouse model. Forty-eight copper/zinc superoxide dismutase mice (strain: B6SJL-TgN [SOD1-G931]1Gur) (SOD1) and 48 control (C) (strain: B6SJL-TgN[SOD1]2Gur) male mice were randomly assigned to four different conditions where 12 SOD1 and 12 C animals were allotted to each condition ( n = 96). Conditions tested the effects of standard housing, a forced exercise regime, access to a mouse house and opportunity for ad libitum exercise on a running wheel. In addition to the daily all-occurrence behavioural sampling, mice were weighed and tested twice per week on gait and Rotor-Rod™ performance until the mice reached the age of 150 days (C) or met the criteria for our humane endpoint (SOD1). The SOD1 mice exposed to the forced exercise regime and wheel access did better in average lifespan and Rotor-Rod™ performance, than SOD1 mice exposed to the standard cage and mouse house conditions. In SOD1 mice, stride length remained longest throughout the progression of the disease in mice exposed to the forced exercise regime compared with other SOD1 conditions. Within the control group, mice in the standard cage and forced exercise regime conditions performed significantly less than the mice with the mouse house and wheels on the Rotor-Rod™. Alpha motor neuron counts were highest in mice with wheels and in mice exposed to forced exercise regime in both mouse strains. All SOD1 mice had significantly lower alpha neuron counts than controls ( P < 0.05). These data show that different enrichment strategies affect behaviour and disease progression in a transgenic mouse model, and may have implications for the effects of these strategies on experimental outcomes.
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Ying, Weihai, Christopher M. Anderson, Yongmei Chen, Becky A. Stein, Christian S. Fahlman, Jean-Christophe Copin, Pak H. Chan, and Raymond A. Swanson. "Differing Effects of Copper, Zinc Superoxide Dismutase Overexpression on Neurotoxicity Elicited by Nitric Oxide, Reactive Oxygen Species, and Excitotoxins." Journal of Cerebral Blood Flow & Metabolism 20, no. 2 (February 2000): 359–68. http://dx.doi.org/10.1097/00004647-200002000-00018.

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Overexpression of Cu,Zn superoxide dismutase (SOD1) reduces ischemic injury in some stroke models but exacerbates injury in a neonatal stroke model and in other settings. The current study used a SOD1 transgenic (SOD1-Tg) murine cortical culture system, derived from the same mouse strain previously used for the stroke models, to identify conditions that determine whether SOD1 overexpression in neurons is protective or detrimental. The nitric oxide (NO) donors S-nitroso- N-acetylpenicillamine, spermine-NONOate, and diethylamine-NONOate produced less death in SOD1-Tg neurons than in wild-type neurons ( p < 0.01). Also, NO produced markedly less 3-nitrotyosine in SOD1-Tg cells. In contrast, the superoxide generator menadione produced significantly greater death and nearly twice as much 2′7′-dichlorofluorescein fluorescence in SOD1-Tg neurons than in wild-type neurons, suggesting increased peroxide formation in the SOD1-Tg cells. No significant difference was observed in the vulnerability of the two cell types to H2O2, the product of the SOD reaction. Over-expression of SOD1 also had no effect on neuronal vulnerability to glutamate, N-methyl-D-aspartate, or kainate. These observations suggest that SOD1 overexpression can reduce neuronal death under conditions where peroxynitrite formation is a significant factor, but may exacerbate neuronal death under conditions of rapid intracellular superoxide formation or impaired H2O2 disposal.
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Nikolić-Kokić, Aleksandra, Zorana Oreščanin-Dušić, Marija Slavić, Ivan Spasojević, Zorica Stević, Mihajlo Spasić, and Duško Blagojević. "The Effects of Human Wild-Type and Fals Mutant L144P SOD1 on Non-Vascular Smooth Muscle Contractions / EFEKTI HUMANE NORMALNE I FALS MUTIRANE L144P SOD1 NA NEVASKULARNE KONTRAKCIJE GLATKIH MIŠIĆA." Journal of Medical Biochemistry 32, no. 4 (October 1, 2013): 375–79. http://dx.doi.org/10.2478/jomb-2013-0032.

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Summary Background: Mutated copper, zinc-containing superoxide dismutase (SOD1) may self-aggregate, an event that could also be an initial cause of motor neuron malfunction leading to disease onset. The effects of human mutated SOD1 pro- tein from the blood of familial amyotrophic lateral sclerosis (FALS) patients bearing Leu144Phe (L144F) mutation were compared to wild-type (WT) human SOD1 derived from healthy examinees, for enzymatic activity and the effects on isometric contractions of non-vascular smooth muscle. Methods: We isolated WT and L144F SOD1 enzymes from eight patients with FALS, L144F mutation in exon 5 and eight healthy controls. We then investigated SOD1 activities in the obtained samples by the adrenaline method and pro- filed them electrophoretically. Finally, we applied WT and L144F SOD1 on the isolated rat uterus. Results: L144F SOD1 showed lower superoxide-dismutating activity compared to WT human SOD1. We found that, in contrast to WT human SOD1, mutated L144F does not induce smooth muscle relaxation. Conclusions: Our data suggest that the lack of relaxation of muscle tonus in the presence of mutated SOD1 may have pathogenic feedback effects in FALS.
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Culik, Robert M., Ashok Sekhar, Jayashree Nagesh, Harmeen Deol, Jessica A. O. Rumfeldt, Elizabeth M. Meiering, and Lewis E. Kay. "Effects of maturation on the conformational free-energy landscape of SOD1." Proceedings of the National Academy of Sciences 115, no. 11 (February 26, 2018): E2546—E2555. http://dx.doi.org/10.1073/pnas.1721022115.

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Amyotrophic lateral sclerosis (ALS) is a devastating fatal syndrome characterized by very rapid degeneration of motor neurons. A leading hypothesis is that ALS is caused by toxic protein misfolding and aggregation, as also occurs in many other neurodegenerative disorders, such as prion, Alzheimer’s, Parkinson’s, and Huntington’s diseases. A prominent cause of familial ALS is mutations in the protein superoxide dismutase (SOD1), which promote the formation of misfolded SOD1 conformers that are prone to aberrant interactions both with each other and with other cellular components. We have shown previously that immature SOD1, lacking bound Cu and Zn metal ions and the intrasubunit disulfide bond (apoSOD12SH), has a rugged free-energy surface (FES) and exchanges with four other conformations (excited states) that have millisecond lifetimes and sparse populations on the order of a few percent. Here, we examine further states of SOD1 along its maturation pathway, as well as those off-pathway resulting from metal loss that have been observed in proteinaceous inclusions. Metallation and disulfide bond formation lead to structural transformations including local ordering of the electrostatic loop and native dimerization that are observed in rare conformers of apoSOD12SH; thus, SOD1 maturation may occur via a population-switch mechanism whereby posttranslational modifications select for preexisting structures on the FES. Metallation and oxidation of SOD1 stabilize the native, mature conformation and decrease the number of detected excited conformational states, suggesting that it is the immature forms of the protein that contribute to misfolded conformations in vivo rather than the highly stable enzymatically active dimer.
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Pytte, Julia, Loren L. Flynn, Ryan S. Anderton, Frank L. Mastaglia, Frances Theunissen, Ian James, Abigail Pfaff, et al. "Disease-modifying effects of an SCAF4 structural variant in a predominantly SOD1 ALS cohort." Neurology Genetics 6, no. 4 (July 1, 2020): e470. http://dx.doi.org/10.1212/nxg.0000000000000470.

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ObjectiveTo test the hypothesis that rs573116164 will have disease-modifying effects in patients with superoxide dismutase 1 (SOD1) familial amyotrophic lateral sclerosis (fALS), we characterized rs573116164 within a cohort of 190 patients with fALS and 560 healthy age-matched controls to assess the variant for association with various measures of disease.MethodsUsing a previously described bioinformatics evaluation algorithm, a polymorphic short structural variant associated with SOD1 was identified according to its theoretical effect on gene expression. An 12–18 poly-T repeat (rs573116164) within the 3′ untranslated region of serine and arginine rich proteins-related carboxy terminal domain associated factor 4 (SCAF4), a gene that is adjacent to SOD1, was assessed for disease association and influence on survival and age at onset in an fALS cohort using PCR, Sanger sequencing, and capillary separation techniques for allele detection.ResultsIn a North American cohort of predominantly SOD1 fALS patients (n =190) and age-matched healthy controls (n = 560), we showed that carriage of an 18T SCAF4 allele was associated with disease within this cohort (odds ratio [OR] 6.6; 95% confidence interval [CI] 3.9–11.2; p = 4.0e-11), but also within non-SOD1 cases (n = 27; OR 5.3; 95% CI 1.9–14.5; p = 0.0014). This finding suggests genetically SOD1-independent effects of SCAF4 on fALS susceptibility. Furthermore, carriage of an 18T allele was associated with a 26-month reduction in survival time (95% CI 6.6–40.8; p = 0.014), but did not affect age at onset of disease.ConclusionsThe findings in this fALS cohort suggest that rs573116164 could have SOD1-independent and broader relevance in ALS, warranting further investigation in other fALS and sporadic ALS cohorts, as well as studies of functional effects of the 18T variant on gene expression.
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Dissertations / Theses on the topic "Cadmium effects on SOD1"

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BOVIO, FEDERICA. "The cadmium altered oxidative homeostasis leads to energetic metabolism rearrangement, Nrf2 activation with increased GSH production and reduced SOD1 activity in neural cells." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2021. http://hdl.handle.net/10281/309982.

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Il cadmio, elemento chimico ampiamente usato in ambito industriale, è considerato un contaminante ambientale con effetti tossici sugli organismi viventi. Il suo ingresso nel corpo umano può avvenire per inalazione o ingestione di cibi ed acqua contaminati, fumo di sigaretta o impiego professionale, con tratto respiratorio e gastrointestinale principalmente coinvolti nel suo assorbimento cellulare. Anche il cervello è un bersaglio della tossicità del cadmio, che può entrare nel sistema nervoso centrale tramite una maggiore permeabilità della barriera ematoencefalica o attraverso i nervi olfattivi. Infatti, l'esposizione al cadmio è stata correlata sia ad alterazioni funzionali del sistema nervoso sia a malattie neurodegenerative, come la sclerosi laterale amiotrofica (SLA). Il 90-95% dei casi di SLA sono sporadici (sALS), mentre il restante 5-10% ha origine familiare (fALS), di cui il 15-20% è attribuito a mutazioni nel gene dell’enzima antiossidante superossido dismutasi 1 (SOD1). SOD1 è un omodimero di 32 kDa, in cui ciascun monomero presenta un ponte disulfuro e due ioni metallici, il rame con ruolo catalitico e lo zinco con funzione strutturale. Poiché uno dei principali meccanismi con cui il cadmio esercita la propria tossicità è lo stress ossidativo, responsabile di un insieme di eventi avversi che culminano nella morte cellulare, scopo di questa tesi è lo studio dell'effetto neurotossico del cadmio sul metabolismo energetico nella linea cellulare umana SH-SY5Y, sulle difese antiossidanti in cellule LUHMES differenziate e sulla funzione di SOD1 in tre modelli sperimentali (proteina ricombinante in E. coli, linea cellulare SH-SY5Y e nematode Caenorhabditis elegans). La valutazione del metabolismo energetico in cellule SH-SY5Y trattate per 24 ore con dosi sub-letali di CdCl2 ha evidenziato il passaggio ad un metabolismo anaerobico; infatti cellule trattate mostrano un aumento della glicolisi, una maggiore produzione di ATP per via glicolitica e una ridotta funzionalità mitocondriale rispetto al controllo. L’apporto bioenergetico in presenza di cadmio non altera la dipendenza da glucosio, ma aumenta quella da glutammina riducendo l’apporto derivato dagli acidi grassi. Inoltre, si osserva un aumento del GSH totale, del rapporto GSSG/GSH e della perossidazione lipidica, tutti indici di un'alterata omeostasi ossidativa. Quest’ultima è stata investigata in cellule LUHMES differenziate, in cui 24 ore di esposizione al cadmio hanno determinato, alle dosi più basse, un aumento del livello di GSH totale e un’attivazione di Nrf2 mediata da p21 e P-Akt. Gli effetti negativi del cadmio sulla vitalità cellulare possono essere annullati dall'aggiunta di GSH e dal trattamento in conditioned medium (CM) ottenuto da astrociti o microglia. Nelle LUHMES trattate in CM il livello totale di GSH rimane paragonabile a quello delle cellule non trattate anche alle concentrazioni più elevate di CdCl2. Infine, l’effetto del cadmio, combinato a dosi fisse di rame e/o zinco, sull'attività catalitica della proteina ricombinante GST-SOD1, espressa in E. coli BL21, ha mostrato una riduzione dose-dipendente dell'attività di SOD1 solo in presenza di rame, mentre il livello di espressione proteica rimane sempre costante. Risultati analoghi sono stati ottenuti nella linea cellulare SH-SY5Y, in cui l'attività enzimatica di SOD1 è diminuita in modo sia dose che tempo-dipendente dopo il trattamento con cadmio per 24 e 48 ore, così come nel nematode C. elegans, in cui si osserva una riduzione del 25% nell’attività di SOD1 dopo 16 ore di trattamento con cadmio. In entrambi i casi il livello di espressione proteica dell’enzima rimane invariato. In conclusione, il cadmio ha determinato il passaggio ad un metabolismo più anaerobico, l'attivazione di Nrf2, con conseguente aumento nella produzione di GSH e una riduzione dell'attività di SOD1.
The heavy metal cadmium is a widespread toxic pollutant, released into the environment mainly by anthropogenic activities. Human exposure can occur through different sources: occupationally or environmentally, with its uptake through inhalation of polluted air, cigarette smoking or ingestion of contaminated food and water. It mainly enters the human body through the respiratory and the gastrointestinal tract and it accumulates in liver and kidneys. Brain is also a target of cadmium toxicity, since this toxicant may enter the central nervous system by increasing blood brain barrier permeability or through the olfactory nerves. In fact, cadmium exposure has been related to impaired functions of the nervous system and to neurodegenerative diseases, like amyotrophic lateral sclerosis (ALS). ALS is a fatal motor neuron pathology with the 90-95% of ALS cases being sporadic (sALS), while the remaining 5-10% of familial onset (fALS); among fALS, the 15-20% is attributed to mutations in superoxide dismutase 1 (SOD1). SOD1 is an antioxidant protein responsible for superoxide anions disruption and it is a homodimeric metalloenzyme of 32 kDa mainly located in the cytoplasm, with each monomer binding one catalytic copper ion and one structural zinc ion within a disulfide bonded conformer. Since oxidative stress is one of the major mechanisms of cadmium induced toxicity and an alteration of oxidative homeostasis, through depletion of antioxidant defences, is responsible for a plethora of adverse outcoming mainly leading to cell death; we focused on cadmium effect (1) on the energetic metabolism in human neuroblastoma SH-SY5Y cell line, (2) on the oxidative defences responses in differentiated human LUHMES neural cell line and (3) on the function of human SOD1 in a three models approach (recombinant protein in E. coli, in SH-SY5Y cell line and in the nematode Caenorhabditis elegans). The evaluation of energetic metabolism of SH-SY5Y neural cells treated with sub-lethal CdCl2 doses for 24 hours, showed an increase in glycolysis compared to control. This shift to anaerobic metabolism has been confirmed by both glycolytic parameters and greater ATP production from glycolysis than oxidative phosphorylation, index of less mitochondrial functionality in cadmium treated cells. Regarding the fuel oxidation cadmium caused an increase in glutamine dependency and a specular reduction in the fatty acids one, without altering the glucose dependency. Moreover, we observed an increase in total GSH, in the GSSG/GSH ratio and in lipid peroxidation, all index of an altered oxidative homeostasis better investigated in LUHMES cells. In this model a 24h cadmium administration enhanced the total GSH content at the lower doses, at which also activates Nrf2 through a better protein stabilization via p21 and P-Akt. The metal adverse effects on cell viability can be rescued by GSH addition and by cadmium treatment in astrocytes- or microglia-conditioned medium. In the latter cases the total GSH level remains comparable to untreated cells even at higher CdCl2 concentrations. Finally, SOD1 catalytical activity has been investigated in the presence of cadmium. The first evaluation of this metal combined with fixed copper and/or zinc on the recombinant GST-SOD1, expressed in E. coli BL21, showed a dose-dependent reduction in SOD1 activity only when copper is added to cellular medium, while the expression remains always constant. Similar results were obtained in SH-SY5Y cell line, in which SOD1 enzymatic activity decreased in a dose- and time-dependent way after cadmium treatment for 24 and 48 hours, without altering its expression; as well as in the Caenorhabditis elegans model, where a 16 hours cadmium treatment caused a 25% reduction only in SOD1 activity. In conclusion, cadmium caused a shift to anaerobiosis, a Nrf2 activation, with increased GSH production, and a reduction in SOD1 activity.
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Jinadasa, K. B. P. Neelantha. "Cadmium effects on vegetables : production, physiology and biochemistry /." View thesis View thesis, 1998. http://library.uws.edu.au/adt-NUWS/public/adt-NUWS20030520.085431/index.html.

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Santos, José António da Costa. "Cadmium effects in Nitzschia Palea frustule proteins." Master's thesis, Universidade de Aveiro, 2010. http://hdl.handle.net/10773/8816.

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Mestrado em Toxicologia e Ecotoxicologia
As diatomáceas são organismos eucarióticos fotossintéticos, cuja relevância como espécies bioindicadoras foi há muito estabelecida, por via de índices ecológicos, ou por via de testes de toxicidade baseados em características ecológicas. A parede celular silicificada (frustula) é a característica mais distintiva destes organismos, permitindo uma identificação da espécie, e fornecendo a indicação de stresses ambientais, devido à indução de formações anormais da frústula. Estas teratologias são a consequência de perturbações no processo de biosilicificação, e podem ocorrer em culturas laboratoriais, ou devido a contaminação por metais, ou pesticidas. De entre os indutores de teratologias, os metais, como o cádmio, são a classe mais relevante devido à sua ocorrência natural ou antropogénica na natureza, e pela sua alta toxicidade relativa às pequenas quantidades presentes. Embora o processo de formação da frustula não esteja ainda completamente esclarecido, nos últimos anos tem sido publicada informação que revela a existência de proteínas na frústula, algumas delas contribuindo para a biosilicificação. O estudo das alterações induzidas pelo cádmio na quantidade, variedade, e relação das proteínas presentes na frústula, foram os objectivos deste trabalho, juntamente com a quantificação de cádmio nas fracções da frústula. Os resultados deste trabalho mostraram que a exposição ao cádmio aumentou o conteúdo proteico da frústula. Cerca de 80% dos peptideos aumentou a expressão na presença de Cd. Este foi sobretudo retido extracelularmente, encontrando-se 85% do Cd ligado a frustulinas. O presente trabalho demonstrou que as frustulinas são extremamente importantes para a defesa da célula dos efeitos do cádmio, contribuindo com dois novos supostos mecanismos de tolerância ao cádmio: o de reforço da frústula, e a protecção celular contra a entrada de Cd, através da quelação extracelular dos iões metálicos. Estes resultados mostram que as frustulinas podem ter um papel importante na tolerância das diatomáceas a metais.
Diatoms are unicellular eukaryotic photosynthetic organisms whose relevance as biomonitor species have long been established, either by ecological indexes, or by tolerance and other toxicity tests, based on ecological properties. The silicified cell wall of diatoms (frustule), is the most visible and distinguished characteristic of these organisms, providing species identification, and indication of environmental stressors, due to the induction of abnormal frustule formation. These teratologies are the consequence of perturbation in the biosilicification process, and can occur either by artificial growth, heavy metal contamination, or pesticides. Amongst the frustule abnormality inductors, metals such as cadmium are the most relevant class due to both anthropogenic and natural occurrence in nature and by the high toxicity relative to the small amounts present in the habitat. Although the process of frustule formation is not completely understood, in the last years it has been published data that show the existence of proteins in the frustules, some of them contributing to the biosilicification. The study of alterations induced by cadmium to the quantity, variety, and ratio of proteins present in frustules were the objectives of this work, along with cadmium quantification in the frustule fractions. Results showed that Cd increased frustule protein content. About 80% of the peptides increased their expression in the presence of Cd . Cadmium was mostly retained extracellularly, and 85% was bound to frustulines. Frustulins were found to be extremely important to the cell defense against cadmium stress, providing two putative novel mechanisms of cadmium tolerance: strengthening of frustules, and protection against Cd, through extracellular metal chelation. These results show that frustulines can play a leading role in the tolerance of diatoms to metals.
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Woods, Scott Andrew. "Behavioral and physiological effects of oxidative stress throughout the lifecycle of Drosophila sod1 mutants." Thesis, University of Iowa, 2017. https://ir.uiowa.edu/etd/6014.

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Oxidative stress has a degenerative effect on neuronal health. Mutations in the copper zinc superoxide dismutase (SOD1), an important antioxidant, have been found in patients suffering from amyotrophic lateral sclerosis (ALS). Classical EMS induced mutations to SOD1 in Drosophila show similar loss of motor coordination and shortened lifespan seen in humans. A study of newly created human ALS point mutants along with the classic alleles show similar phenotypes in their neurodegeneration. I examined markers of oxidative stress, neuronal health and behavioral phenotypes throughout the lifecycle of aging flies. Larvae were largely found to be unaffected by mutations in SOD1, with no measured increase in ROS level over wild type (WT) flies. Mutant pupae were found to have two major defects in their circadian eclosion rhythm and their fundamental ability to eclose from the pupal casing. Adults showed the classic reduced lifespan and motor abilities. To further examine the health on non-glutamatergic synapses electroretinograms (ERGs) were recorded at different levels of survivorship indicated by Kaplan-Meier Survival curves. These ERGs show that the histaminergic synapses they record have greater degeneration in aging SOD1 mutants than in WT flies. This is true for their chronological age as well as their biological age. There was coinciding disruption of the photo transduction pathway of the photoreceptors that coincided with degeneration at the synapse. This demonstrates the separate degenerative effect of high levels of oxidative stress impart separate for the normal aging process.
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Hanson, Miranda Leah. "Prenatal cadmium exposure dysregulates sonic hedgehog and Wnt/beta-catenin signaling in the thymus resulting in immunomodulatory effects." Morgantown, W. Va. : [West Virginia University Libraries], 2009. http://hdl.handle.net/10450/10625.

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Thesis (Ph. D.)--West Virginia University, 2009.
Title from document title page. Document formatted into pages; contains vii, 250 p. : ill. (some col.). Vita. Includes abstract. Includes bibliographical references.
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Jinadasa, N., of Western Sydney Hawkesbury University, of Science Technology and Agriculture Faculty, and School of Horticulture. "Cadmium effects on vegetables : production, physiology and biochemistry." THESIS_FSTA_HOR_Jinadasa_K.xml, 1998. http://handle.uws.edu.au:8081/1959.7/456.

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Cadmium (Cd) is absorbed through the lungs and the digestive tract; however, for most human non-smokers, the major route of Cd entry into the body is by ingestion. Perhaps 5% of ingested Cd is absorbed and once absorbed, Cd accumulates mostly in the liver and kidneys, where it can cause a variety of health problems. This applies equally to grazing stock. The major entry point of Cd into the food chain is therefore uptakes of traces of Cd by crop plants. This thesis focuses on Cd in vegetables. The study was conducted in an Australian context, where geogenic Cd contributions to soils are typically low. Most of the Cd in soils on Australian vegetable farms originates from materials added to boost crop production. Phosphate fertilisers were and remain the dominant Cd source. Most Australian soils are P-deficient and high rates of P fertiliser are essential for successful vegetable cropping. The P fertilisers used throughout Australia were formerly made from guano deposits mined on Pacific Islands. These contained high percentages of Cd. Current rock sources contain lower Cd concentrations. Studies showed that all the vegetable samples which contained excessive Cd concentrations were leafy vegetables, including cabbage, lettuce, silverbeet, parsley and bok choy. Cadmium impaired photosynthesis; reduced dry weight of the whole plant; slowed leaf elongation rate; decreased the length of fully expanded leaves; slowed the rate at which new leaves appeared; and altered foliar concentrations of Zn, Mn, Cu, Ca and S. These profound changes affected all parts of the plant; consequently, Cd did not affect the proportion of dry weight partitioned to the roots, stems and leaves.
Doctor of Philosophy (PhD)
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Brandt, Clarissa. "The Effects of Cadmium and Lead on Phaseolus vulgaris." University of the Western Cape, 2012. http://hdl.handle.net/11394/5096.

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Magister Scientiae (Biodiversity and Conservation Biology) - MSc (Biodiv and Cons Biol)
The demand for better quality produce by consumers is on the increase, as higher heavy metal concentrations pose a problem in agriculture. They result in decreased yield and unsuitable food for human consumption. This brings about a negative economic effect as such products become unprofitable on the domestic or export markets thus affecting productivity of farms.Four heavy metals (Cd, Cu, Pb and Zn) have been shown to be a problem in the farming areas in Cape Town. Pot and field studies were carried out on the effects and concentrations of cadmium and lead on Phaseolus vulgaris. Field studies included collecting plant samples from the Joostenbergvlakte/ Kraaifontein farming areas and measuring the heavy metal concentrations within the different organs of the plants. Pot experiments were carried out, where Phaseolus vulgaris var. Contender were grown and then heavy metals were administered to these plants together with two heavy metal mitigation techniques, precipitation with phosphate and mobilisation with EDTA to see if they were successful in combating heavy metal pollution.Samples taken from farms in the Joostenbergvlakte/ Kraaifontein area revealed that cadmium, lead and zinc concentrations were higher than the legal standard in the edible fruits. In the pot experiment, results revealed that cadmium reduced the chlorophyll index as well as the shoot fresh mass and changes in mineral uptake were seen. Lead did not affect growth or the chlorophyll index. The high cadmium treatment resulted in a marked increase in sodium concentration in the shoots. The phosphate treatments and EDTA treatments both resulted in increased cadmium concentrations in the roots and shoots. The higher phosphate and lead treatments also reduced lead concentrations in the roots. Low phosphate and the EDTA treatments increased the shoot sodium concentrations.
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Pinho, Francisco Carvalho Vieira. "Cytotoxic and genotoxic effects of cadmium in human osteoblasts." Master's thesis, Universidade de Aveiro, 2011. http://hdl.handle.net/10773/8061.

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Mestrado em Biologia Aplicada - Biologia Molecular e Celular
Due to industrialization, cadmium has been increasingly accumulated in soil, water and air, and consequently the food chain, thus, being responsible for many diseases. In humans, damages to several organs and carcinogenic effects take place. However, the mechanisms underlying the bone diseases remain unknown, and so, this work aims to evaluate cytotoxic and genotoxic effects of cadmium in human osteoblasts cell line MG-63. Cells were exposed to 0 μM, 20 μM and 50 μM CdCl2 for 24 and 48 hours. Cell proliferation / viability was determined by the MTT assay, cell cycle effects were evaluated by flow cytometry, and DNA damage was assessed by the comet assay. After both times of exposure, cell viability decreased in both cadmium doses, although cell cycle progression alterations were not detected. However, cadmium lead to clastogenic effects and DNA damage in cells exposed to the cadmium dose of 50 μM, for 48 h. In conclusion, at 20 μM and 50 μM and for the periods tested cadmium chloride induced cytotoxic and genotoxic effects on MG-63 cell line, as it decreased cell viability, induced DNA damage and clastogenicity, though it did not change cell cycle progression.
Devido à industrialização, a contaminação ambiental por metais como o cádmio tem aumentado no solo, água e ar. Consequentemente, a cadeia alimentar é afetada e, desta forma, o cádmio surge como agente carcinogénico e como causador de algumas doenças relacionadas com lesões em vários órgãos. Contudo, os mecanismos subjacentes a doenças ósseas ainda não se encontram totalmente desvendados, e assim neste trabalho, pretende-se avaliar os efeitos citotóxicos e genotóxicos do cádmio em osteoblastos humanos, na linha celular MG-63. As células foram expostas a 0 μM, 20 μM e 50 μM de cloreto de cádmio durante 24 e 48 horas. A proliferação / viabilidade celular foi avaliada pelo ensaio MTT, os efeitos na progressão do ciclo celular por foram avaliados por citometria de fluxo e os danos no DNA pelo ensaio de cometas. Após ambos os tempos de exposição a 20 μM e 50 μM de cloreto de cádmio, as células sofreram uma diminuição da viabilidade celular e não foram observadas alterações na progressão do ciclo celular. No entanto, o cádmio conduziu a efeitos clastogénicos e danos no DNA em células expostas à concentração de 50 μM, após 48 h de exposição. Concluindo, as concentrações 20 μM e 50 μM de cloreto de cádmio para os períodos testados, induziram efeitos citotóxicos e genotóxicos nas células da linha MG-63, dado que conduziram a uma diminuição da sua viabilidade, danos no DNA e clastogenicidade, não havendo, contudo, alterações na progressão do ciclo celular.
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Haider, Syed Raza. "Effects of chronic cadmium exposure on macrophage function in mice." Thesis, University of Essex, 1989. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.236639.

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Школьна, Ірина Іванівна, Ирина Ивановна Школьная, Iryna Ivanivna Shkolna, Андрій Миколайович Лобода, Андрей Николаевич Лобода, Andrii Mykolaiovych Loboda, Віталій Едуардович Маркевич, Виталий Эдуардович Маркевич, and Vitalii Eduardovych Markevych. "Protective role of the placenta against toxic effects of cadmium." Thesis, Sumy State University, 2016. http://essuir.sumdu.edu.ua/handle/123456789/46325.

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The placenta has a number of features that ensure the passage of many biological substances to the fetus, as well as the function of barrier for certain substances. According to researchers, it can be used as a marker of unfavorable environmental action.
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Books on the topic "Cadmium effects on SOD1"

1

A, Bernard, and Foulkes Ernest C. 1924-, eds. Cadmium. Berlin: Springer-Verlag, 1986.

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1907-, Mislin Hans, and Ravera O, eds. Cadmium in the environment. Basel: Birkhäuser, 1986.

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C, Pappas A., ed. Cadmium toxicity and the antioxidant system. Hauppauge, N.Y: Nova Science, 2010.

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McKenzie, Joan. Cadmium intake via oysters and health effects in New Zealand: Cadmium intake, metabolism, and effects in people with a high intake of oysters in New Zealand. Research Triangle Park, NC: U.S. Environmental Protection Agency, Health Effects Research Laboratory, 1986.

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McKenzie, Joan. Cadmium intake via oysters and health effects in New Zealand: Cadmium intake, metabolism, and effects in people with a high intake of oysters in New Zealand. Research Triangle Park, NC: U.S. Environmental Protection Agency, Health Effects Research Laboratory, 1986.

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Dier-Ackley, Liisa. Effects of cadmium and zinc on the germination of mung beans (Vigna radiata). Bellingham, WA: Huxley College of Environmental Studies, Western Washington University, 1998.

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IARC Working Group on the Evaluation of Carcinogenic Risks to Humans (1993 Lyon, France). Beryllium, cadmium, mercury, and exposures in the glass manufacturing industry. Lyon: IARC, 1993.

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Gunnar, Nordberg, Herber R. F. M, Alessio L, International Agency for Research on Cancer., International Union of Pure and Applied Chemistry., and Università di Brescia. Institute of Occupational Health., eds. Cadmium in the human environment: Toxicity and carcinogenicity. Lyon: International Agency for Research on Cancer ; New York : Distributed in the USA by Oxford University Press, 1992.

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Matović, Vesna. Zinc, copper, or magnesium supplementation against cadmium toxicity. Hauppauge, N.Y: Nova Science, 2010.

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Matović, Vesna. Zinc, copper, or magnesium supplementation against cadmium toxicity. New York: Nova Science, 2010.

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Book chapters on the topic "Cadmium effects on SOD1"

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Nordberg, Gunnar F., Teruhiko Kido, and Harry A. Roels. "Cadmium-induced renal effects." In Clinical Nephrotoxins, 785–810. Boston, MA: Springer US, 2008. http://dx.doi.org/10.1007/978-0-387-84843-3_35.

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Kido, Teruhiko, Gunnar F. Nordberg, and Harry A. Roels. "Cadmium-induced renal effects." In Clinical Nephrotoxins, 507–30. Dordrecht: Springer Netherlands, 2003. http://dx.doi.org/10.1007/1-4020-2586-6_25.

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Flick, Karin, and Peter Kaiser. "Cellular Mechanisms to Respond to Cadmium Cadmium Exposure: Ubiquitin Ligases." In Cellular Effects of Heavy Metals, 275–89. Dordrecht: Springer Netherlands, 2011. http://dx.doi.org/10.1007/978-94-007-0428-2_13.

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Hallenbeck, William H. "Human health effects of exposure to cadmium." In Cadmium in the Environment, 131–37. Basel: Birkhäuser Basel, 1986. http://dx.doi.org/10.1007/978-3-0348-7238-6_17.

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Cox, R. M. "Contamination and effects of cadmium in native plants." In Cadmium in the Environment, 101–9. Basel: Birkhäuser Basel, 1986. http://dx.doi.org/10.1007/978-3-0348-7238-6_13.

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Bernard, A., and R. Lauwerys. "Effects of Cadmium Exposure in Humans." In Handbook of Experimental Pharmacology, 135–77. Berlin, Heidelberg: Springer Berlin Heidelberg, 1986. http://dx.doi.org/10.1007/978-3-642-70856-5_5.

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Nishijo, Muneko, and Hideaki Nakagawa. "Effects of Cadmium Exposure on Life Prognosis." In Current Topics in Environmental Health and Preventive Medicine, 63–73. Singapore: Springer Singapore, 2019. http://dx.doi.org/10.1007/978-981-13-3630-0_5.

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McGrath, S. P. "Adverse Effects of Cadmium on Soil Microflora and Fauna." In Cadmium in Soils and Plants, 199–218. Dordrecht: Springer Netherlands, 1999. http://dx.doi.org/10.1007/978-94-011-4473-5_8.

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Matysik, J., Alial, H. J. van Gorkom, and H. J. M. de Groot. "Substitution of Calcium By Cadmium in Photosystem II Complex." In Photosynthesis: Mechanisms and Effects, 1423–26. Dordrecht: Springer Netherlands, 1998. http://dx.doi.org/10.1007/978-94-011-3953-3_336.

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Bánfalvi, Gáspár. "Cellular Changes in Mammalian Cells Induced by Cadmium." In Cellular Effects of Heavy Metals, 147–62. Dordrecht: Springer Netherlands, 2011. http://dx.doi.org/10.1007/978-94-007-0428-2_6.

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Conference papers on the topic "Cadmium effects on SOD1"

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Hui Li and Nanning Duan. "Effects on the rice seedling growth by cadmium tolerant bacteria under cadmium stress." In 2011 International Conference on Remote Sensing, Environment and Transportation Engineering (RSETE). IEEE, 2011. http://dx.doi.org/10.1109/rsete.2011.5965930.

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Wurm, Patrick, Makram Hage-Ali, Jean M. Koebel, Christiane Ritt, and Paul Siffert. "Afterglow effects in cadmium telluride radiation detectors." In SPIE's 1994 International Symposium on Optics, Imaging, and Instrumentation, edited by Elena Aprile. SPIE, 1994. http://dx.doi.org/10.1117/12.187263.

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Cornelius, L. K., P. A. Tick, and N. F. Borelli. "Photochromic/photoconductive effects in cadmium-alumino fluorosilicates." In Bragg Gratings, Photosensitivity, and Poling in Glass Fibers and Waveguides. Washington, D.C.: Optica Publishing Group, 1997. http://dx.doi.org/10.1364/bgppf.1997.jsue.24.

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A novel interaction was observed in cadmium-alumino fluorosilicate glasses when exposed to near UV radiation. Glasses high in cadmium were observed to be photochromic. Accompanying the darkening process was a change of up to five orders of magnitude in the DC conductivity. The process involved the formation of the cadmous ion (Cd+1) as an electron trap. A thin, transparent conductive skin could also be formed by appropriate heat treatments.
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Raita, Erik, Alexei A. Kamshilin, Oleg Kobozev, and Aleksandr Shumelyuk. "Germanium doped cadmium telluride crystals for optical sensing." In Photorefractive Effects, Materials, and Devices. Washington, D.C.: OSA, 2001. http://dx.doi.org/10.1364/pemd.2001.344.

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Huang, Hui, Rui-min Wan, Zeng-lin Zhao, Rong-bin Ji, and Shun-chen Pan. "Growth and structure of cadmium zinc telluride crystal." In Photorefractive Effects, Materials, and Devices. Washington, D.C.: OSA, 2005. http://dx.doi.org/10.1364/pemd.2005.26.

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Lin, Lijin, Zhihui Wang, and Loao Liao. "Effects of DTPA on Cadmium Accumulation of Galinsoga parviflora." In 2015 3rd International Conference on Advances in Energy and Environmental Science. Paris, France: Atlantis Press, 2015. http://dx.doi.org/10.2991/icaees-15.2015.170.

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Zhao, Jing, and Yuhui Qiao. "The Effects of Cadmium on Soil Free Living Nematodes." In 2008 2nd International Conference on Bioinformatics and Biomedical Engineering. IEEE, 2008. http://dx.doi.org/10.1109/icbbe.2008.615.

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Huang, Jiajing, Lijin Lin, Lei Yuan, and Ming'an Liao. "Effects of Paclobutrazol on Cadmium Accumulation of Stellaria Media." In 2016 2nd International Conference on Advances in Energy, Environment and Chemical Engineering (AEECE 2016). Paris, France: Atlantis Press, 2016. http://dx.doi.org/10.2991/aeece-16.2016.24.

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Odoulov, S. G., K. V. Shcherbin, A. N. Shumelyuk, P. M. Fochuk, and O. E. Panchuk. "Electron-hole competition in dynamic hologram recording in cadmium telluride." In Photorefractive Materials, Effects, and Devices II. Washington, D.C.: Optica Publishing Group, 1993. http://dx.doi.org/10.1364/pmed.1993.frc.3.

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It is well known that noncentrosymmetric cubic semiconductor crystals offer the possibility of the recording of shifted dynamic gratings due to diffusion charge transport which in turn leads to intensity coupling of two recording waves [1,2].
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Verstraeten, D., Ph C. Lemaire, and J. C. Launay. "Bridgman growth and electric breakdown behavior of Vanadium-Zinc codoped Cadmium Telluride." In Photorefractive Effects, Materials, and Devices. Washington, D.C.: OSA, 2001. http://dx.doi.org/10.1364/pemd.2001.558.

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Reports on the topic "Cadmium effects on SOD1"

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Zimmerman, A. H. Effects of Cadmium Electrode Properties on Nickel-Cadmium Cell Performance. Fort Belvoir, VA: Defense Technical Information Center, December 1987. http://dx.doi.org/10.21236/ada191394.

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Sacco-Gibson, N., J. Abrams, S. Chaudhry, D. Hurst, D. Peterson, and M. Bhattacharyya. Osteoporotic-like effects of cadmium on bone mineral density and content in aged ovariectomized beagles. Office of Scientific and Technical Information (OSTI), December 1992. http://dx.doi.org/10.2172/10185066.

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Craig, K. D., K. Burnett, A. Ringwood, K. MacDougal, and L. Kendall. The effects of cadmium of the growth and metallothionein expression of the bivalve larvae, crassostrea virginica. Office of Scientific and Technical Information (OSTI), December 1994. http://dx.doi.org/10.2172/121302.

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Petersen, Michael David. Numerical Simulation of the Performance Characteristics, Instability, and Effects of Band Gap Grading in Cadmium Telluride Based Photovoltaic Devices. Office of Scientific and Technical Information (OSTI), January 2001. http://dx.doi.org/10.2172/804001.

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Petersen, Michael David. Numerical Simulation of the Performance Characteristics, Instability, and Effects of Band Gap Grading in Cadmium Telluride Based Photovoltaic Devices. Office of Scientific and Technical Information (OSTI), May 2001. http://dx.doi.org/10.2172/797338.

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Desiderati, Christopher. Carli Creek Regional Water Quality Project: Assessing Water Quality Improvement at an Urban Stormwater Constructed Wetland. Portland State University, 2022. http://dx.doi.org/10.15760/mem.78.

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Stormwater management is an ongoing challenge in the United States and the world at-large. As state and municipal agencies grapple with conflicting interests like encouraging land development, complying with permits to control stormwater discharges, “urban stream syndrome” effects, and charges to steward natural resources for the long-term, some agencies may turn to constructed wetlands (CWs) as aesthetically pleasing and functional natural analogs for attenuating pollution delivered by stormwater runoff to rivers and streams. Constructed wetlands retain pollutants via common physical, physicochemical, and biological principles such as settling, adsorption, or plant and algae uptake. The efficacy of constructed wetlands for pollutant attenuation varies depending on many factors such as flow rate, pollutant loading, maintenance practices, and design features. In 2018, the culmination of efforts by Clackamas Water Environment Services and others led to the opening of the Carli Creek Water Quality Project, a 15-acre constructed wetland adjacent to Carli Creek, a small, 3500-ft tributary of the Clackamas River in Clackamas County, OR. The combined creek and constructed wetland drain an industrialized, 438-acre, impervious catchment. The wetland consists of a linear series of a detention pond and three bioretention treatment cells, contributing a combined 1.8 acres of treatment area (a 1:243 ratio with the catchment) and 3.3 acre-feet of total runoff storage. In this study, raw pollutant concentrations in runoff were evaluated against International Stormwater BMP database benchmarks and Oregon Water Quality Criteria. Concentration and mass-based reductions were calculated for 10 specific pollutants and compared to daily precipitation totals from a nearby precipitation station. Mass-based reductions were generally higher for all pollutants, largely due to runoff volume reduction on the treatment terrace. Concentration-based reductions were highly variable, and suggested export of certain pollutants (e.g., ammonia), even when reporting on a mass-basis. Mass load reductions on the terrace for total dissolved solids, nitrate+nitrite, dissolved lead, and dissolved copper were 43.3 ± 10%, 41.9 ± 10%, 36.6 ± 13%, and 43.2 ± 16%, respectively. E. coli saw log-reductions ranging from -1.3 — 3.0 on the terrace, and -1.0 — 1.8 in the creek. Oregon Water Quality Criteria were consistently met at the two in-stream sites on Carli Creek for E. coli with one exception, and for dissolved cadmium, lead, zinc, and copper (with one exception for copper). However, dissolved total solids at the downstream Carli Creek site was above the Willamette River guidance value 100 mg/L roughly 71% of the time. The precipitation record during the study was useful for explaining certain pollutant reductions, as several mechanisms are driven by physical processes, however it was not definitive. The historic rain/snow/ice event in mid-February 2021 appeared to impact mass-based reductions for all metals. Qualitatively, precipitation seemed to have the largest effect on nutrient dynamics, specifically ammonia-nitrogen. Determining exact mechanisms of pollutant removals was outside the scope of this study. An improved flow record, more targeted storm sampling, or more comprehensive nutrient profiles could aid in answering important questions on dominant mechanisms of this new constructed wetland. This study is useful in establishing a framework and baseline for understanding this one-of-a-kind regional stormwater treatment project and pursuing further questions in the future.
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