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Nitric oxide (NO) and melatonin are two biostimulant molecules in plants that not only modulate the growth and development of plants but also confer enhanced tolerance to abiotic stresses. Therefore, in this study, the interactive effects of melatonin and nitric oxide (NO) on seedlings of Catharanthus roseus (L.) G. Don was evaluated under both control and conditions of stress due to Cd. Our results show that both melatonin and sodium nitroprusside (SNP, as an NO donor) significantly improved seedling growth, which was associated with the enhanced concentration of photosynthetic pigments in both the control plants and under Cd-stress conditions. Impacts of both melatonin and SNP were more pronounced in the Cd-stressed plants than control seedlings. The Cd stress increased [H.sub.2][O.sub.2] and lipid peroxidation levels in roots. Melatonin, as well as SNP, increased endogenous NO concentration in roots. Both melatonin and SNP enhanced the concentration of proline and the activities of antioxidant enzymes (SOD, POD, APX, CAT) and lowered [H.sub.2][O.sub.2] and lipid peroxidation levels in roots of C. roseus plants under Cd stress. These melatonin-induced responses in the roots were suppressed by 4-carboxyphenyl-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (cPTIO; a specific scavenger of NO), but inhibition of melatonin biosynthesis by p--chlorophenylalanine, could not reverse the protective effects conferred by NO. These outcomes suggest that NO, as a downstream signaling molecule, is implicated in the melatonin-promoted antioxidant responses in roots of C. roseus plants. Key words: antioxidative defense, cadmium, Catharanthus roseus, melatonin, nitric oxide. L'oxyde nitrique (NO) et la melatonine sont deux molecules biostimulantes chez les vegetaux qui, non seulement, modulent la croissance et le developpement des plantes, mais leur conferent aussi une tolerance accrue aux stress abiotiques. Ainsi, dans cette etude, l'effet interactif de la melatonine et du NO sur des semis de Catharanthus roseus (L.) G. Don a ete evalue sous des conditions contrôle et de stress provoque par le Cd. Les resultats ont montre que la melatonine et le nitroprussiate de sodium (NPS comme donneur de NO) amelioraient significativement la croissance des semis qui etait associee a une concentration accrue de pigments photosynthetiques tant en condition contrôle que sous un stress provoque par le Cd. Les impacts de la melatonine et du NPS etaient plus prononces sur les plants stresses par le Cd que les semis contrôles. Le stress provoque par le Cd augmentait les niveaux de [H.sub.2][O.sub.2] et de peroxydation lipidique dans les racines. La melatonine de meme que le NPS augmentaient la concentration de NO endogene dans les racines. La melatonine et le NPS augmentaient la concentration de proline et l'activite d'enzymes antioxydantes (SOD, POD, APX et CAT) et diminuaient les niveaux de [H.sub.2][O.sub.2] et de peroxydation lipidique dans les racines des plants de C. roseus en condition de stress provoque par le Cd. Ces reponses induites par la melatonine dans les racines etaient supprimees par le 4-carboxyphenyl-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxyde (cPTIO, un piegeur specifique de NO), mais l'inhibition de la biosynthese de melatonine par la p-chlorophenylalanine ne pouvait renverser les effets protecteurs conferes par le NO. Ces resultats montrent que le NO, en tant que signal en aval, est implique dans les reponses antioxydantes favorisees par la melatonine dans les racines de plants de C. roseus. [Traduit par la Redaction] Mots-cles: defense antioxydante, cadmium, Catharanthus roseus, melatonine, oxyde nitrique., Introduction Cadmium is an extremely toxic heavy metal that enters agricultural soils, especially in developing countries, via the application of urban composts, phosphate fertilizers, metal-based pesticides, ripening agents, and waste-water [...]

Cadmium (Cd) contamination in soil has become a serious worldwide environmental and health problem. Cd is easily taken up by plants and translocated to aboveground tissues. A pot experiment was carried out to explore the role of the ascorbate-glutathione (AsA-GSH) cycle and endogenous hormones in enhancing Cd tolerance and promoting translocation of Cd in one-year-old seedlings of Populus x euramericana 'Neva'. The antioxidant substances ascorbic acid (AsA), dehydroascorbic acid (DHA), glutathione (GSH), and oxidized glutathione (GSSG); the activities of the antioxidant enzymes ascorbic acid peroxidase (APX), glutathione reductase (GR), monodehydroascorbate reductase (MDHAR), and dehydroascorbic acid reductase (DHAR); the levels of the endogenous hormones indole-3-acetic acid (IAA), abscisic acid (ABA), gibberellin (G[A.sub.3]), and zeatin riboside (ZR); and the contents of malondialdehyde (MDA) and hydrogen peroxide ([H.sub.2][O.sub.2]) were investigated after 30 days of irrigation with half-Hoagland solution containing 0 or 100 [micro]mol*[L.sup.-1] Cd[(N[O.sub.3]).sub.2] under magnetic treatment (MT) or nonmagnetic treatment (NMT). The results were as follows. (i) Compared with NMT, MT increased the AsA levels in roots compared with those in leaves under Cd stress, whereas it increased the DHA levels in the leaves but decreased the DHA levels in the roots. The GSH and GSSG levels both increased by 8%-151% under MT. (ii) MT inhibited the APX activity in blades and roots, and a similar effect was observed on the foliar activities of GR and MDHAR, with a decrease of 8%-50%; however, MT increased the activation of DHAR in the blades and GR in the roots. In addition, compared with NMT, MT increased the activities of GR, MDHAR, and DHAR by 19%-285% in Populus (poplar). (iii) With the exogenous addition of Cd, the Cd accumulation and biological transport coefficient of Cd from roots to leaves (S/R) were enhanced in poplar, accompanied by increased levels of [H.sub.2][O.sub.2] and MDA due to MT. (iv) The levels of IAA, ABA, GA, and ZR were inhibited by 19%-95% in the leaves following MT. In contrast, the levels of these endogenous hormones were increased by 18%-203% in the roots following MT. (v) MT improved the seedling growth of poplar, with an increase of 0.4%-90%, compared with that of the NMT. The ground diameter and number of root tips showed the greatest increases, with average ratios of 29% and 87%, respectively. These results suggested a large increase in AsA and decreases in poplar antioxidant enzymes, especially in the leaves, with a high GSH level. In this review, we concluded that the antioxidant substance GSH plays an important role in the AsA-GSH cycle following exposure to a magnetic field under Cd stress. Additionally, the roots play a major role in eliminating oxygen free radicals by regulating the levels and ratios of various endogenous hormones. Moreover, magnetization could alleviate Cd-induced oxidative stress by stimulating MDHAR, DHAR, and GR activities; enhance the defense capability of the AsA-GSH cycle; and maintain normal physiological metabolism in poplar. Key words: cadmium stress, magnetization, antioxidant substance, antioxidant enzymes, endogenous hormone. La contamination des sols par le cadmium (Cd) est devenue un serieux probleme environnemental et sanitaire partout dans le monde. Le Cd est facilement absorbe par les plantes et transporte vers les parties aeriennes. Une experience en pot a ete realisee pour etudier le role du cycle de l'ascorbate-glutathion (AsA-GSH) et des hormones endogenes dans l'augmentation de la tolerance au Cd et la promotion de la translocation du Cd chez des semis de Populus x euramericana 'Neva'. Les substances antioxydantes telles que l'acide ascorbique (AsA), l'acide dehydroascorbique (DHA), le glutathion (GSH), et le glutathion oxyde (GSSG); l'activite des enzymes antioxydantes telles que l'acide ascorbique peroxydase (APX), la glutathion reductase (GR), la monodehydroascorbique reductase (MDHAR) et l'acide dehydroascorbique reductase (DHAR); le niveau des hormones endogenes telles que l'acide 3-indole acetique (IAA), l'acide abscisique (ABA), la gibberelline (G[A.sub.3]) et la zeatine riboside (ZR); et la teneur en malonaldehyde (MDA) et en peroxyde d'hydrogene ([H.sub.2][O.sub.2]) ont ete etudies apres 30 jours d'irrigation avec une solution de Hoagland diluee de moitie contenant 0 ou 100 [micro]mol*[L.sup.-1] de Cd[(N[O.sub.3]).sub.2] avec (MT) ou sans (NMT) traitement magnetique. Voici les resultats. (i) Relativement a NMT, MT a augmente la teneur en AsA dans les racines comparativement a ce qui a ete observe dans les feuilles en presence d'un stress du au Cd, tandis qu'il a augmente la teneur en DHA dans les feuilles mais l'a diminue dans les racines. MT a augmente de 8 a 151 % les teneurs en GSH et GSSG. (ii) MT a inhibe l'activite de l'APX dans les limbes et les racines et un effet semblable a ete observe dans le cas de l'activite foliaire de la GR et de la MDHAR entrainant une diminution de 8 a 50%; cependant, MT a augmente l'activite de la DHAR dans les limbes et celle de la GR dans les racines. De plus, comparativement a NMT, MT a augmente de 19 a 285 % l'activite de la GR, de la MDHAR et de la DHAR chez le peuplier (Populus). (iii) L'ajout exogene de Cd a favorise l'accumulation de Cd et augmente le coefficient de transport biologique de Cd des racines vers les feuilles (S/R) chez le peuplier, accompagne par une augmentation des teneurs en [H.sub.2][O.sub.2] et MDA a cause de MT. (iv) Les teneurs en IAA, ABA, G[A.sub.3] et ZR ont ete reduites de 19 a 95 % dans les feuilles a la suite de MT. Par contre MT a augmente de 18 a 203 % la teneur en hormones endogenes dans les racines. (v) MT a augmente de 0,4 a 90 % la croissance des semis de peuplier comparativement a NMT. Le diametre au sol et le nombre d'apex racinaires ont connu la plus forte augmentation, soit des ratios respectifs de 29 et 87 %. Ces resultats indiquent que l'AsA connait une forte augmentation et que l'activite des enzymes antioxydantes diminue chez le peuplier, particulierement dans les feuilles, avec une teneur elevee en GSH. Dans cette revue de litterature, nous arrivons a la conclusion que la substance antioxydante GSH joue un role important dans le cycle de l'AsA-GSH a la suite d'une exposition a un champ magnetique en presence d'un stress du au Cd. En outre, les racines jouent un role majeur dans l'elimination des radicaux libres d'oxygene en controlant les niveaux et les ratios d'une variete d'hormones endogenes. De plus, la magnetisation pourrait attenuer le stress oxydatif induit par le Cd en stimulant l'activite de la MDHAR, de la DHAR et de la GR, en ameliorant la capacite de defense du cycle de l'AsA-GSH et en maintenant un metabolisme physiologique normal chez le peuplier. [Traduit par la Redaction] Mots-cles: stress du au cadmium, magnetisation, substance antioxydante, enzymes antioxydantes, hormone endogene., Introduction Cadmium (Cd) is a nonessential nutrient for plant growth and is one of the most biotoxic heavy metal elements (Gallego et al. 2012; Cornu et al. 2016). Cd pollution [...]

Introduction Cadmium is a heavy metal pollutant derived from several industrial activities, such as the production of batteries and pigment for paint production; it is also a contaminant in cigarette [...], In the kidney, the accumulation of heavy metals such as [Cd.sup.2+] produces mitochondrial dysfunctions, i.e., uncoupling of the oxidative phosphorylation, inhibition of the electron transport through the respiratory chain, and collapse of the transmembrane electrical gradient. This derangement may be due to the fact that [Cd.sup.2+] induces the transition of membrane permeability from selective to nonselective via the opening of a transmembrane pore. In fact, [Cd.sup.2+] produces this injury through the stimulation of oxygen-derived radical generation, inducing oxidative stress. Several molecules have been used to avoid or even reverse [Cd.sup.2+]-induced mitochondrial injury, for instance, cyclosporin A, resveratrol, dithiocarbamates, and even EDTA The aim of this study was to explore the possibility that the antioxidant tamoxifen could protect mitochondria from the deleterious effects of [Cd.sup.2+]. Our results indicate that the addition of 1 [micro]mol/L [Cd.sup.2+] to mitochondria collapsed the transmembrane electrical gradient, induced the release of cytochrome c, and increased both the generation of [H.sub.2][O.sub.2] and the oxidative damage to mitochondrial DNA (among other measured parameters). Of interest, these mitochondrial dysfunctions were ameliorated after the addition of tamoxifen. Key words: mitochondria, kidney, cadmium, oxidative stress, permeability transition. Dans le rein, l'accumulation de metaux lourds comme le [Cd.sup.2+] provoque des dysfonctionnements mitochondriaux c'est-a-dire le decouplage de la phosphorylation oxydative, l'inhibition du transport des electrons a travers la chaine respiratoire et l'effondrement de gradient electrique transmembranaire. Ce dereglement peut etre du au fait que le [Cd.sup.2+] induit la transition de la permeabilite membranaire d'un etat selectif a un etat non selectif au moyen de l'ouverture des pores transmembranaires. En fait, le [Cd.sup.2+] produit ce dommage par la stimulation de la generation de radicaux libres d'oxygene menant a un stress oxydant. Plusieurs molecules ont ete utilisees pour eviter ou meme renverser le dommage aux mitochondries induit par le [Cd.sup.2+], par exemple, la cyclosporine A, le resveratrol, les dithiocarbamates et meme l'EDTA. L'objectif de la presente etude etait d'explorer la possibilite que le tamoxifene, un antioxydant, puisse preserver la fonction mitochondriale des effets nocifs du [Cd.sup.2+]. Les resultats des auteurs indiquent que l'ajout de 1 [micro]mol/L de [Cd.sup.2+] a des mitochondries provoquait l'effondrement du gradient electrique transmembranaire, induisait la liberation de cytochrome c et augmentait la production de [H.sub.2][O.sub.2] et le dommage oxydant a l'ADN mitochondrial (parmi d'autres parametres mesures). Fait interessant, ces dysfonctionnements mitochondriaux etaient attenues a la suite de l'ajout de tamoxifene. [Traduit par la Redaction] Mots-cles: mitochondrie, rein, cadmium, stress oxydant, transition de permeabilite.

A variety of factors affect the release of the mugineic acid family of phytosiderophores (PS) from the roots of graminaceous plants. We investigated the effects of copper (Cu) toxicity with or without cadmium (Cd) toxicity on PS release in barley (Hordeum vulgare L. cv. Minorimugi). To characterise the effect of Cu toxicity on PS release, 10 µmol [L.sup.-1] Cu (a 100-fold higher concentration than the control condition) was added to the plant culture medium. The results showed that PS release from the roots was stimulated in response to Cu toxicity. In a second experiment, 5 µmol x [L.sup.-1] Cu was added to the medium with or without the addition of 5 µmol x [L.sup.-1] Cd. In this experiment, the release of PS was drastically reduced in response to Cd. We suggest that Cu toxicity in barley is a signal that activates PS release by plant roots, whereas PS release induced by Cu toxicity is strongly attenuated by Cd toxicity. We propose that inhibition of PS release could be one of the harmful effects of Cd toxicity in plants. Our results provide new information about one of the responses of graminaceous plants to heavy metal stress. Key words: cadmium, copper, graminaceous plants, phytosiderophores, response, toxicity. Resume: Divers facteurs influent sur la liberation de l'acide mugineique, de la famille des phytosiderophores (PS), provenant des racines des plantes graminees. Nous avons etudie les effets de la toxicite du cuivre (Cu) avec ou sans la toxicite du cadmium (Cd) sur la liberation de PS dans l'orge (Hordeum vulgare L. cv. Minorimugi). Dix µmol x [L.sup.-1] de Cu (100 fois plus eleves que la condition de controle) ont ete appliques au milieu pour caracteriser la toxicite induite par le Cu et la liberation de PS chez les plantes. Dans une seconde experience, 5 µmol x [L.sup.-1] de Cu ont ete appliques au milieu avec ou sans 5 µmol x [L.sup.-1] de Cd. La quantite de PS liberee des racines etait elevee en reponse a la toxicite du Cu. Cependant, la liberation de PS etait radicalement reduite en raison de la presence concomitante de Cd. Nous suggerons que la toxicite du Cu dans l'orge agit comme un signal qui active la liberation de PS des racines de la plante, tandis que la liberation de PS induite par la toxicite du Cu est tres vulnerable a l'exces de Cd. Nous considerons que l'inhibition de la liberation de PS pourrait constituer l'un des effets nefastes du Cd sur les plantes. Nos resultats fournissent de nouvelles informations sur l'une des reponses des plantes graminees au stress du aux metaux lourds. Mots-cles: cadmium, cuivre, plantes graminees, phytosiderophores, reponse, toxicite., Introduction The mugineic acid family of phytosiderophores (PS) are non-proteinogenic secondary amino acids capable of chelating ferric iron (Fe) (Takagi 1976; Takagi et al. 1984). Graminaceous plants possess a unique [...]

Cadmium toxicity and reactive oxygen species Cadmium is an occupationally and environmentally important toxic element that is present in the air, soil, sediment, and water. Non-occupational exposure is mainly from [...], We provide an overview of our studies on cadmium and the actin cytoskeleton in mesangial cells, from earlier work on the effects of [Cd.sup.2+] on actin polymerization in vivo and in vitro, to a role of disruption or stabilization of the cytoskeleton in apoptosis and apoptosis-like death. More recent studies implicate cadmium-dependent association of gelsolin and the [Ca.sup.2+]/calmodulin-dependent protein kinase II (CaMK-II) with actin filaments in cytoskeletal effects. We also present previously unpublished data concerning cadmium and the disruption of focal adhesions. The work encompasses studies on rat, mouse, and human mesangial cells. The major conclusions are that [Cd.sup.2+] acts independently of direct effects on cellular [Ca.sup.2+] levels to nevertheless activate [Ca.sup.2+]-dependent proteins that shift the actin polymerization-depolymerization in favour of depolymerization. Cadmium-dependent translocation of CaMK-IIS, gelsolin, and a 50 kDa gelsolin cleavage fragment to the filamentous (F-)actin cytoskeleton appear to be involved. An intact filamentous actin cytoskeleton is required to initiate apoptotic and apoptotic-like death, but F-actin depolymerization is an eventual result. Key words: cadmium toxicity, actin polymerization, cytoskeleton, calcium/calmodulin-dependent protein kinase-II, gelsolin, apoptosis, reactive oxygen species, mesangial cell. Nous presentons un survol des etudes que nous avons realisees sur le cadmium et le cytosquelette d'actine dans les cellules mesangiales, de nos premiers travaux sur les effets du [Cd.sup.2+] sur la polymerisation de l'actine in vivo et in vitro, jusqu'a un role de la desintegration ou la stabilisation du cytosquelette dans la mort par apoptose ou de type apoptose. Des etudes plus recentes impliquent l'association dependante du cadmium de la gelsoline et de la proteine kinase dependante du [Ca.sup.2+]/calmoduline II (CaMKII) aux filaments d'actine dans les effets du cytosquelette. Nous presentons aussi des donnees anterieures non publiees qui concernent le cadmium et l'interruption des adhesions focales. Ces travaux comprennent des etudes sur les cellules mesangiales du rat, de la souris et de l'humain. Les principales conclusions sont que le [Cd.sup.2+] agit independamment des effets directs sur les niveaux de [Ca.sup.2+] cellulaire pour activer malgre tout des proteines dependantes du [Ca.sup.2+] qui deplacent l'equilibre polymerisation-depolymerisation en faveur de la depolymerisation. La translocation dependante du cadmium de la CaMK-IIS,de la gelsoline et d'un fragment de 50 kDa issu du clivage de la gelsoline vers le cytosquelette d'actine filamenteuse (F-) semble impliquee. Un cytosquelette intact d'actine filamenteuse est requis pour initier la mort par apoptose ou de type apoptose, mais la depolymerisation de la F-actine est un resultat a long terme. [Traduit par la Redaction] Mots-cles : toxicite du cadmium, polymerisation de l'actine, cytosquelette, proteine kinase dependante du [Ca.sup.2+]/calmoduline II, gelsoline, apoptose, espece reactive d'oxygene, cellule mesangiale.

Introduction Mercury, lead, and cadmium are found in the environment either as naturally occurring metals or as a result of anthropogenic activities. All have the ability to cross the maternal [...], The study described in this article aimed to determine if measurable levels of mercury, lead, and cadmium are detected in the umbilical cord blood specimens collected in a community hospital in Rhode Island and if prenatal exposure correlates with prematurity or fetal growth indicators. Total mercury, lead, and cadmium concentrations were measured in 538 specimens of cord blood and correlated with demographic characteristics and pregnancy outcomes for each mother-infant pair. Lead concentrations determined in the cord blood of Rhode Island women (geometric mean 0.99 [micro]g/dL) were similar to those reported in U.S. biomonitoring studies. The overall geometric mean for mercury concentration (0.52 [micro]g/L) was slightly lower than in other comparable studies. Cadmium concentrations were generally below the limit of detection. A statistically significant correlation was detected between elevated mercury concentrations and racial and ethnic characteristics of the study participants. Non-Hispanic African-American mothers were 9.6 times more likely to have a mercury concentration [greater than or equal to]5.8 [micro]g/L compared to women of other racial/ethnic backgrounds. No association was detected between elevated mercury levels and adverse birth outcomes.

ABSTRACT This work concerns the effects of cadmium exposure on the anaerobic and oxidative metabolism in tissues of the hypoxia-tolerant green mussel Perna viridis from Venezuelan coastal waters. The mussels [...]

Problem statement: Defining of correlation between toxic and essential elements in human beings is an important clinical screening procedure. Approach: The aim of this study was to determine the correlation between cadmium as toxic element and calcium as an essential element in the blood at the smokers. We have investigated 50 human blood samples of different ages and genders (age: 35-45 years old), of the citizens from the Municipality of Dragash (an environment without pollution). Results: The results that were achieved in this study showed the significant difference in the average of cadmium concentration in human blood of the smokers group from nonsmokers group (p = Conclusion/Recommendations: Correlation between [Cd.sup.2+] and [Ca.sup.2+] in the human blood with a high statistical significance in the group of smokers comes as a result of powerful competitive reaction between [Cd.sup.2+] and [Ca.sup.2+] in biochemical processes. Competitive reaction between [Cd.sup.2+] and [Ca.sup.2+] in biochemical processes. Key words: Cadmium, calcium, smoking, blood, INTRODUCTION Cadmium is one of the most commonly found toxic metals present in our environment. The major route of exposure to cadmium for the general non-smoking population is via food, [...]

Benthic marine organisms such as mollusks are often exposed to periodic oxygen deficiency (due to the tidal exposure and/or seasonal expansion of the oxygen-deficient dead zones) and pollution by metals [e.g., cadmium, (Cd)]. These stressors can strongly affect mollusks' survival; however, physiological mechanisms of their combined effects are not fully understood. We studied the effects of Cd exposure on metabolic responses to prolonged anoxia and subsequent recovery in anoxia-tolerant intertidal mollusks Crassostrea virginica (eastern oysters). Anoxia led to an onset of anaerobiosis indicated by accumulation of L-alanine, acetate, and succinate. Prolonged anoxia (for 6 days) caused a decline in the maximum activity of electron transport chain and ADP-stimulated (state 3) oxygen uptake by mitochondria (M[O.sub.2]), but no change in the resting (state 4) M[O.sub.2] of oyster mitochondria, along with a slight but significant reduction of mitochondrial respiratory control ratio. During reoxygenation, there was a significant overshoot of mitochondrial M[O.sub.2] (by up to 70% above the normoxic steady-state values) in control oysters. Mild mitochondrial uncoupling during prolonged shutdown in anoxic tissues and a subsequent strong stimulation of mitochondrial flux during recovery may help to rapidly restore redox status and protect against elevated reactive oxygen species formation in oysters. Exposure to Cd inhibits anaerobic metabolism, abolishes reoxygenation-induced stimulation of mitochondrial M[O.sub.2], and leads to oxidative stress (indicated by accumulation of DNA lesions) and a loss of mitochondrial capacity during postanoxic recovery. This may result in increased sensitivity to intermittent hypoxia and anoxia in Cd-exposed mollusks and will have implications for their survival in polluted estuaries and coastal zones. air exposure; recovery; mitochondrial function; oxidative damage; mollusks doi: 10.1152/ajpregu.00324.2009.

Cadmium is a highly toxic environmental contaminant that has been implicated in various disorders. A major mechanism for cadmium detoxification in the yeast Saccharomyces cerevisiae relies on extrusion via Pca1, a P-type ATPase. While an N-terminal degron targets Pca1 for degradation before its secretion to the plasma membrane, cadmium in the growth media rapidly upregulates Pca1 by preventing its turnover. Here we show that the endoplasmic reticulum-associated degradation (ERAD) system, known for its role in quality control of secretory proteins, is unexpectedly responsible for the regulation of Pca1 expression by cadmium. Direct cadmium sensing at the ER by a degron in Pca1 leads to an escape of Pca1 from ERAD. This regulated conversion of an ERAD substrate to a secretory competent state in response to a cellular need illustrates a mechanism for expressional control of a plasma membrane protein. Yeast has likely evolved this mode of regulation for a rapid response against cadmium toxicity at the expense of constant synthesis and degradation of Pca1. ERAD of a portion of secretory proteins might occur via signal-dependent regulatory mechanisms as demonstrated for Pca1. ERAD | degron | P-type ATPase | Pca1 yeast

Marine ectotherms, including oysters are exposed to variable environmental conditions in coastal shallow waters and estuaries. In the light of global climate change, additional stressors like pollution might pose higher risk to populations. On the basis of the concept of oxygen- and capacity-limited thermal tolerance in aquatic ectotherms (40), we show that a persistent pollutant, cadmium, can have detrimental effects on oysters (Crassostrea virginica). During acute warming from 20 to 28[degrees]C (4[degrees]C/48 h) standard metabolic rate (SMR) rose in control and cadmium-exposed (50 [micro]g [Cd.sup.2+]/1) animals, with a consistently higher SMR in Cd-exposed oysters. Additionally, Cd-exposed oysters showed a stronger temperature-dependent decrease in hemolymph oxygen partial pressures. This observation indicates that the effect of temperature on aerobic metabolism was exacerbated due to the additional Cd stress. The oxygen delivery systems could not provide enough oxygen to cover Cd-induced elevated metabolic demands at high temperatures. Interestingly, cardiac performance (measured as the heart rate and hemolymph supply to tissues) rose to a similar extent in control and Cd-exposed oysters with warming indicating that cardiac output was unable to compensate for elevated energy demand in Cd-exposed oysters. Together with the literature data on metal-induced reduction of ventilatory capacity, these findings suggest that synergistic effects of elevated temperatures and cadmium exposure led to oxygen limitation by impaired performance in oxygen supply through ventilation and circulation. Overall, cadmium exposure resulted in progressive hypoxemia in oysters at high temperatures, suggesting that the thermal tolerance window is narrowed in marine ectotherms inhabiting polluted areas compared with pristine environments. aerobic metabolism; cardiac performance; magnetic resonance imaging, hemolymph [Po.sub.2], anaerobiosis

In the adult rat, chronic cadmium intoxication induces nephropathy with Fanconi-like features. This result raises the question of whether intoxication of pregnant rats has any deleterious effects on renal function in their offspring. To test this hypothesis, we measured the renal function of 2- to 60-day-old postnatal offspring from female rats administered cadmium chloride by the oral route (0.5 rag. [kg.sup.-1] [day.sup.-1) throughout their entire gestation. Investigations of rat offspring from contaminated pregnant rats showed the presence of cadmium in the kidney at gestational day 20. After birth, the cadmium kidney concentration increased from postnatal day 2 to clay 60 (PND2 to PND60), presumably because of 1) milk contamination and 2) neonatal liver cadmium content release. Although the renal parameters (glomerular filtration, U/P inulin, and urinary excretion rate) were not significantly affected until PND45, renal failure appeared at PND60, as demonstrated by a dramatic decrease of the glomerular filtration rate associated with increased excretion of the main ions. In parallel, an immunofluorescence study of tight-junction protein expression of PND60 offspring from contaminated rats showed a disorganization of the tight-junction proteins claudin-2 and claudin-5, specifically expressed in the proximal tubule and glomerulus, respectively. In contrast, expression of a distal claudin protein, claudin-3, was not affected. In conclusion, in utero exposure of cadmium leads to toxic renal effects in adult offspring. These results suggest that contamination of pregnant rats is a serious and critical hazard for renal function of their offspring. heavy metals; renal failure; newborn; claudins

The nephrotoxic metal cadmium at micromolar concentrations induces apoptosis of rat kidney proximal tubule (PT) cells within 3-6 h of exposure. The underlying cell death pathways remain poorly defined. Using Hoechst 33342/ ethidium bromide nuclear staining and 3-(4,5-dimethyl-2-thiazolyl) 2,5-diphenyl-2H-tetrazolium bromide (MTT) cell death assays, 10-50 [micro]M cadmium induced apoptosis of immortalized rat kidney cells derived from the S1-segment of PT at 6 and 24 h, but necrosis at 24 h only. Cadmium (10-50 [micro]M) also caused mitochondrial cytochrome c (cyt. c)- and apoptosis-inducing factor release at 24 h, but not at 6 h, as measured by immunofluorescence imaging and immunoblotting. Caspases-9 and -3 were activated only by l0 [micro]M cadmium for 24 h, and accordingly apoptosis was significantly reduced by the respective inhibitors (z-LEHD-fmk, z-DEVD-fmk; 10 [micro]g/ml) at 24 h, but not at 6 h, without affecting necrosis. At 6 h, 10 [micro]M cadmium increased the activity of the calcium-activated protease calpain, but not at 24 h, and calpain inhibitors (ALLN, PD 150606; 10-30 [micro]M) blocked apoptosis by 10 [micro]M cadmium at 3-6 h. However, PD-150606 also attenuated caspase-3 activity and apoptosis at 24 h, suggesting calpain-dependent caspase activation. Thus cadmium-induced apoptosis of PT cells involves a complex and sensitive interplay of signaling cascades involving mitochondrial proapoptotic factors, calpains and caspases, whose activation is also determined by cadmium concentration and the duration of cadmium exposure. heavy metals; apoptosis-inducing factor; cytochrome c; cysteine proteases

The environmental pollutant cadmium affects human health, with the kidney being a primary target. In addition to proximal tubules, glomeruli and their contractile mesangial cells have also been identified as targets of cadmium nephrotoxicity. Glomerular contraction is thought to contribute to reduced glomerular filtration, a characteristic of cadmium nephrotoxicity. Because p38 MAPK/HSP25 signaling has been implicated in smooth muscle contraction, we examined its role in cadmium-induced contraction of mesangial cells. We report that exposure of mesangial cells to cadmium resulted in 1) cell contraction, 2) activation of MAP kinases, 3) increased HSP25 phosphorylation coincident with p38 MAP kinase activation, 4) sequential phosphorylation of the two phosphorylation sites of mouse HSP25 with Ser15 being phosphorylated before Ser86, 5) reduction of oligomeric size of HSP25, and 6) association of HSP25 with microfilaments. Exposure of isolated rat glomeruli to cadmium also resulted in contraction and increased HSP25 phosphorylation. The cadmium-induced responses were inhibited by the specific p38 MAP kinase inhibitor SB-203580, and cadmium-induced phosphorylation of HSP25 was inhibited by expression of a dominant-negative p38 MAP kinase mutant. These findings tentatively suggest that cadmium-induced nephrotoxicity results, in part, from glomerular contraction due to p38 MAP kinase/ HSP25 signaling-dependent contraction of mesangial cells. With regard to the cellular action of HSP25, these data support a change in paradigm: in addition to its weII-established cytoprotective function, HSP25 may also be involved in processes that ultimately lead to adverse effects, as is observed in the response of mesangial cells to cadmium. cadmium nephrotoxicity; actin; microfilaments; phosphorylation

Cadmium and zinc are removed from cells of Ralstonia metallidurans by the CzcCBA efflux pump and by two soft-metal-transporting P-type ATPases, CadA and ZntA. The czcCBA genes are located on plasmid pMOL30, and the cadA and zntA genes are on the bacterial chromosome. Expression of zntA from R. metallidurans in Escherichia coli predominantly mediated resistance to zinc, and expression of cadA predominantly mediated resistance to cadmium. Both transporters decreased the cellular content of zinc or cadmium in this host. In the plasmid-free R. metallidurans strain AE104, single gene deletions of cadA or zntA had only a moderate effect on cadmium and zinc resistance, but zinc resistance decreased 6-fold and cadmium resistance decreased 350-fold in double deletion strains. Neither single nor double gene deletions affected zinc resistance in the presence of czcCBA. In contrast, cadmium resistance of the cadA zntA double mutant could be elevated only partially by the presence of CzcCBA. lacZ reporter gene fusions indicated that expression of cadA was induced by cadmium but not by zinc in R. metallidurans strain AE104. In the absence of the zntA gene, expression of cadA occurred at lower cadmium concentrations and zinc now served as an inducer. In contrast, expression of zntA was induced by both zinc and cadmium, and the induction pattern did not change in the presence or absence of CadA. However, expression of both genes, zntA and cadA, was diminished in the presence of CzcCBA. This indicated that CzcCBA efficiently decreased cytoplasmic cadmium and zinc concentrations. It is discussed whether these data favor a model in which the cations are removed either from the cytoplasm or the periplasm by CzcCBA.

DMT1 (divalent metal transporter 1) is a hydrogen-coupled divalent metal transporter with a substrate preference for iron, although the protein when expressed in frog oocytes transports a broad range of metals, including the toxic metals cadmium and lead. Wild-type Caco-2 cells displayed saturable transport of lead and iron that was stimulated by acid. Cadmium and manganese inhibited transport of iron, but zinc and lead did not. The involvement of DMT1 in the transport of toxic metals was examined by establishing clonal DMT1 knockdown and control Caco-2 cell lines. Knockdown cell lines displayed much lower levels of DMT1 mRNA and a smaller [V.sub.max] for iron uptake compared with control cell lines. One clone was further characterized and found to display an ~50% reduction in uptake of iron across a pH range from 5.5 to 7.4. Uptake for cadmium also decreased 50% across the same pH range, but uptake for lead did not. These results show that DMT1 is important in iron and cadmium transport in Caco-2 cells but that lead enters these cells through an independent hydrogen-driven mechanism. divalent metal transporter 1; transport; intestine

Research has been conducted on Streptococcus thermophilus strain 4134. The identification of the cadmium resistance cassete on the genome of this strain has been carried out, and the model for expression regulation of cadmium resistence in lactic acidic bacteria is described.

Water-soluble luminescent CdS quantum dots (QDs) capped by polyphosphate, L-cysteine, and thioglycerol were synthesized in aqueous solution. The ligands were found to have a profound effect on the luminesence response of CdS QDs to physiologically important metal cations. Polyphosphate-capped CdS QDs were sensitive to nearly all mono- and divalent cations, showing no ion selectivity. Conversely, thioglycerol-capped CdS QDs were sensitive to only copper and iron ions. Similar concentrations of physiologically relevant cations, such as zinc, sodium, potassium, calcium, and magnesium ions did not affect the luminescence of thioglycerol-capped CdS QDs. On the other hand, L-cysteine-capped CdS QDs were sensitive to zinc ions and insensitive to other physiologically important cations, such as copper, calcium, and magnium ions. To demonstrate the detection capability of these new ion probes, L-cysteine and thioglycerolcapped CdS QDs were used to detect zinc and copper ions in physiological buffer samples. The detection limits were 0.8 [micro]M for zinc (II) and 0.1 [micro]M for copper (II) ions. The emission enhancement of the QDs by zinc (II) is attributed to activation of surface states, whereas the effective reduction of copper (II) to copper (I) may explain the emission decrease of the thioglycerol-capped CdS QDs when charged with copper ions. Unlike organic fluorescent dyes, the thioglycerol-capped luminescent CdS QDs discriminate between copper and zinc ions and are therefore suitable for the analysis of copper ions in biological samples in the presence of physiological concentrations of zinc ions. The interference of iron ions with zinc and copper ion detection is attributed to an inner filter effect, which is eliminated by adding fluoride ions to form the colorless complex Fe[F.sub.6.sup.3-]. To the best of our knowledge, this is first use of luminescent semiconductor quantum dots as selective ion probes in aqueous samples.

Research has been conducted on the cadmium(II) arenedisulfonate compounds. These compounds have been obtained from aqueous solution and structurally characterized by IR spectroscopy, thermal gravimetric analysis and X-ray single-crystal diffraction.

Research has been conducted on the inorganic/organic coordination polymers. The synthesis of these polymers carried out via the use of the rigid ligand 1,2-bis(3-pyridyl)ethyne (3,3'-DPA) is described.

Research has been conducted on the inorganic oxyfluoride chains. The hydrogen bonding occurring between these chains and the role of the racemic (inversion) twin formation have been investigated and the details are reported.

Research has been conducted on the metal cyclam complexes. The antiviral activity of these complexes has been investigated and results indicate their biological activity depends on membrane protein recognition and configurations.

Research has been conducted on the coordination polymer assembly and design. The study of the two-dimensional rhombohedral grid coordination polymers has been carried out and the polymers' third-order nonlinear optical properties have been determined via the use of Z-scan technique in the N,N-dimethylformamide solution.

Research has been conducted on the electron-transfer reaction in single mutants. Results demonstrate the combined effects of Cd (super)2+ binding and point mutations on the mutants' cumulative consequence which decreases the electron-transfer rates.