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Titolo:
Renal cortical mitochondrial dysfunction upon cadmium metallothionein administration to Sprague-Dawley rats
Autore:
Tang, WF; Shaikh, ZA;
Indirizzi:
Univ Rhode Isl, Coll Pharm, Dept Biomed Sci, Kingston, RI 02881 USA Univ Rhode Isl Kingston RI USA 02881 t Biomed Sci, Kingston, RI 02881 USA
Titolo Testata:
JOURNAL OF TOXICOLOGY AND ENVIRONMENTAL HEALTH-PART A
fascicolo: 3, volume: 63, anno: 2001,
pagine: 221 - 235
SICI:
1528-7394(20010608)63:3<221:RCMDUC>2.0.ZU;2-V
Fonte:
ISI
Lingua:
ENG
Soggetto:
POTATO-TUBER MITOCHONDRIA; OXIDATIVE-PHOSPHORYLATION; INDUCED NEPHROPATHY; LIVER MITOCHONDRIA; EXPOSED RATS; CALCIUM-IONS; NEPHROTOXICITY; METABOLISM; TRANSPORT; KIDNEY;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Agriculture,Biology & Environmental Sciences
Life Sciences
Citazioni:
49
Recensione:
Indirizzi per estratti:
Indirizzo: Shaikh, ZA Univ Rhode Isl, Coll Pharm, Dept Biomed Sci, 41 Lower Coll Rd, Kingston, RI 02881 USA Univ Rhode Isl 41 Lower Coll Rd Kingston RI USA 02881 02881 USA
Citazione:
W.F. Tang e Z.A. Shaikh, "Renal cortical mitochondrial dysfunction upon cadmium metallothionein administration to Sprague-Dawley rats", J TOX E H A, 63(3), 2001, pp. 221-235

Abstract

A bolus dose of cadmium metallothionein (CdMT) produces renal proximal tubular dysfunction because it accumulates in the tubular epithelial cells andundergoes rapid degradation, releasing Cd. Morphologically, mitochondria appear to be the target organelle. The present study examined changes in renal cortical mitochondrial function following CdMT administration and investigated whether some of these effects could be ascribed to Cd2+ accumulationin the mitochondria. Sprague-Dawley rats were injected ip with 0.3 mg Cd as CdMT/kg and the animals were sacrificed after 6, 8, or 12 h. Two- to threefold increases in urinary protein excretion and LDH activity were evident at 8 h, with marked elevations (11- and 29-fold) thereafter. Renal corticalmitochondria were swollen and rounded at IZ h. The mitochondrial Cd level was 399 pmol/mg protein at 6 h and did not change significantly during the next 6 h: however, mitochondrial respiratory function declined with time. At 12 h, state 3 oxygen consumption, respiratory control ratio (RCR), and ADP:O (P/O) ratio were 48, 49, and 76% of control values, respectively, indicating inhibition of electron transfer and oxidative phosphorylation. The direct effect of Cd on mitochondrial function was examined by incubating mitochondria from untreated rats with 0.1-2 muM CdCl2. Rapid uptake of Cd resulted in concentration-dependent effects on respiration. After 1 min of incubation with 2 muM Cd, the mitochondria contained 262 mu gCd/mg protein and state 3 respiration and RCR values were 75 and 33% of control levels, respectively Thus, renal proximal tubular cell damage following a bolus dose of CdMT involves perturbations in mitochondrial respiration, brought on by the accumulation of Cd.

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Documento generato il 04/04/20 alle ore 15:19:48