Distribution of cadmium and metallothionein in CdCl<sub>2</sub>‐exposed rat kidney: Relationship with apoptosis and regeneration

Tanimoto, Akihide; Hamada, Tetsuo; Higashi, Ken; Sasaguri, Yasuyuki

doi:10.1046/j.1440-1827.1999.00833.x

Cited by 17 publications

(11 citation statements)

References 27 publications

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“…According to Ribelin and Migiaki (1975), and Tanimoto et al (1999) cadmium is responsible for the pathological changes of kidney tubules, and these findings were also confirmed by the results of our investigation related to the kidneys of fish that were purposely poisoned during the experimental stage. (see Figures 4,5,6 and 7).…”

Section: Discussionsupporting

confidence: 89%

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Beširović¹,

Alić²,

Prašović³

et al. 2010

Turk. J. Fish. Aquat. Sci.

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The aim of the present study was to investigate the histopathological changes on the organs of the brown trout (Salmo trutta m. fario) inflicted by per oral cadmium and zinc poisoning in the 46-week experimental period. The fish were kept in well-oxygenated freshwater basins which were purposely set for the experiment. During the investigation, we set up two experimental basins along with the control one. We put 30 specimens of one-year-old brown trout of the average weight of 15 grams in each basin. According to Venugopal, peroral toxic doses for fish can not be determined precisely. Accurate lethal doses (LD 50 and LD) can only be established for a number of laboratory animals. However, it is possible to calculate the approximate toxic doses for fish from peroral lethal doses for rats. The calculated values for cadmium chloride are 4,4 mg/kg and 11 mg/kg for zinc sulphate, respectively. In the experimental stage we soaked the fish food in solutions made in conformity with the aforementioned values of cadmium chloride and zink sulphate. As a result, the fish consumed the aforementioned toxic doses in the experimental stage, considering that the feeding regimen included the food ration of 2% body weight/day.Keywords: Heavy metals, fish, peroral poisoning, histopathological. Kronik Uygulanan Kadmiyum ve Çinkoya Maruz Kalan Kahverengi Alabalığın (Salmo trutta m. fario) Böbrek ve Solungaçlarına Histopatolojik Etkileri ÖzetBu çalışmanın amacı, 46 haftalık deney süresinde beher kadmiyum ve çinko zehirlenmesine uğrayan kahverengi alabalığın (Salmo trutta m. fario) organları üzerindeki histopatolojik değişiklikleri belirlemektir. Balıklar, deney için oluşturulan oksijenli tatlı su havzalarında muhafaza edilmiştir. Araştırma süresince kontrol bölgeyle birlikte iki deney havzası oluşturulmuştur. Her havzaya ortalama ağırlığı 15 gram olan, 30 adet ve bir yaşında kahverengi alabalık koyulmuştur. Venugopal'a göre balıklar için peroral toksik dozlar tam olarak tespit edilemez. Kesin ölümcül dozlar (LD 50 ve LD) yalnızca birkaç laboratuar hayvanı için tespit edilebilir. Fakat fareler için olan peroral ölümcül dozlardan, balıklar için yaklaşık toksik dozlar hesaplamak mümkündür. Hesaplanan değerler sırasıyla kadmiyum klorür için 4,4 mg/kg ve çinko sülfat için 11 mg/kg'dır. Deneysel aşamada sözü edilen kadmiyum klorür ve çinko sülfat değerlerine uygun olarak hazırlanan çözeltide balık yemi bekletilmiştir. Sonuç olarak beslenme rejiminin %2 vücut ağırlığı/gün yem rasyonu içerdiği dikkate alındığında balıklar deneysel aşamada bahsi geçen toksik dozları tüketmiştir.Anahtar Kelimeler: Ağır metaller, balık, oral zehirlenme dozu, histopatolojik etki.

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Section: Discussionsupporting

confidence: 89%

Untitled

Beširović¹,

Alić²,

Prašović³

et al. 2010

Turk. J. Fish. Aquat. Sci.

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“…However, it has also been apparent that early manifestations of cadmiuminduced proximal tubule dysfunction occur well before the onset of necrosis. In the 1990s, several investigators (Hamada et al, 1991;Tanimoto et al, 1993Tanimoto et al, , 1999Yan et al, 1997) published results showing that the early stages of cadmium nephrotoxicity were associated with an increase in the number of apoptotic cells in the proximal tubule. In each of these studies, there was no significant evidence of necrotic injury at the time that apoptosis was observed.…”

Section: Role Of Necrosis Apoptosis and Autophagy In Cadmium Nephromentioning

confidence: 99%

Mechanisms of Cadmium-Induced Proximal Tubule Injury: New Insights with Implications for Biomonitoring and Therapeutic Interventions

Prozialeck

Edwards

2012

J Pharmacol Exp Ther

220

150

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Cadmium is an important industrial agent and environmental pollutant that is a major cause of kidney disease. With chronic exposure, cadmium accumulates in the epithelial cells of the proximal tubule, resulting in a generalized reabsorptive dysfunction characterized by polyuria and low-molecular-weight proteinuria. The traditional view has been that as cadmium accumulates in proximal tubule cells, it produces a variety of relatively nonspecific toxic effects that result in the death of renal epithelial cells through necrotic or apoptotic mechanisms. However, a growing volume of evidence suggests that rather than merely being a consequence of cell death, the early stages of cadmium-induced proximal tubule injury may involve much more specific changes in cell-cell adhesion, cellular signaling pathways, and autophagic responses that occur well before the onset of necrosis or apoptosis. In this commentary, we summarize these recent findings, and we offer our own perspectives as to how they relate to the toxic actions of cadmium in the kidney. In addition, we highlight recent findings, suggesting that it may be possible to detect the early stages of cadmium toxicity through the use of improved biomarkers. Finally, some of the therapeutic implications of these findings will be considered. Because cadmium is, in many respects, a model cumulative nephrotoxicant, these insights may have broader implications regarding the general mechanisms through which a variety of drugs and toxic chemicals damage the kidney.

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“…For example, metaloxine(8-hydroxyquinoline) complexes are known to emit yellow-green fluorescence and this fluorescence method is presently used for detecting cadmium in tissues, although its staining sensitivity is comparable with the QAI method (Hamada et al, 1991;Tanimoto et al, 1999). Recently, extremely sensitive fluorescent chelating agents have been developed for detecting calcium in cells.…”

Section: Perspective and Conclusionmentioning

confidence: 99%

Recent advances in the histochemical staining of heavy metals by means of chelating agents, with special reference to cadmium

Sumi

Suzuki

2002

Microscopy Res & Technique

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This review discusses the way of improving the sensitivity and specificity of chelating agents used for the histochemical demonstration of trace amounts of heavy metals in cells and tissues. In the search for a more sensitive and specific agent, various chelating agents have been prepared and their staining properties for various metals examined. Of those developed 1-(2-benzothiazolylazo)-2-naphthol (BTAN), 2-(8-quinolylazo)-4,5-(diphenyl)imidazole (QAI), and 2-(5-bromo-2-pridylazo)-5-(diethylamino)phenol (BrPADAP) were far superior to conventional staining agents in staining sensitivity. This was particularly so for staining cadmium. When modifying chelating agents to increase staining sensitivity, hydrophobicity of the agent molecules, selection of substituent groups, and the position of the groups added to the agent molecules must be taken into consideration. The most frequently mentioned factors in a staining mechanism are complex-tissue attractive forces, and recent studies have made it clear that weak interactions, such as hydrogen bonds and hydrophobic interactions, contribute significantly. The Hansch pi values were a useful indication of the hydrophobicity of metal staining agents. The published values for stability constants of metal complexes were found to be unreliable guides for choosing a masking agent to block interfering metals. The polyphosphates, aminopolycarboxylic acids, and alkylamines were among the most useful masking agents for metal staining from a practical standpoint.

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Distribution of cadmium and metallothionein in CdCl₂‐exposed rat kidney: Relationship with apoptosis and regeneration

Cited by 17 publications

References 27 publications

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Untitled

Mechanisms of Cadmium-Induced Proximal Tubule Injury: New Insights with Implications for Biomonitoring and Therapeutic Interventions

Recent advances in the histochemical staining of heavy metals by means of chelating agents, with special reference to cadmium

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Distribution of cadmium and metallothionein in CdCl2‐exposed rat kidney: Relationship with apoptosis and regeneration

Cited by 17 publications

References 27 publications

Untitled

Untitled

Mechanisms of Cadmium-Induced Proximal Tubule Injury: New Insights with Implications for Biomonitoring and Therapeutic Interventions

Recent advances in the histochemical staining of heavy metals by means of chelating agents, with special reference to cadmium

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Distribution of cadmium and metallothionein in CdCl₂‐exposed rat kidney: Relationship with apoptosis and regeneration