Comparative cytotoxic responses of cultured avian and rodent aortic smooth muscle cells to allylamine

Kenneth Ramos, C. H. Thurlow

Research output: Contribution to journalArticle

7 Citations (Scopus)

Abstract

The present studies were designed to compare the acute cytotoxic responses of cultured avian and rodent aortic smooth muscle cells (SMCs) to allylamine (AAM), a selective vascular toxin. SMCs were isolated from male Japanese quail or Sprague-Dawley rats and established in culture by standard procedures. Cellular glutathione (GSH) content and lactate dehydrogenase (LDH) leakage were used as indices of cytotoxicity. Exposure of avian and rodent SMCs in primary culture to AAM (0.2-200 μM) for 4 h was associated with a significant reduction in cellular GSH and enzyme leakage in cultures of both cell types. Increased exposure time to 24 h further depleted cellular GSH levels and enhanced the leakage of LDH in primary cultures of avian SMCs. In contrast, enhanced LDH leakage occurred without further GSH depletion in primary cultures of rodent SMCs upon exposure to AAM for 24 h. Removal of serum did not modulate the cytotoxic response profile of primary cultures of avian SMCs treated with 200 μM AAM, but was associated with marked elevation in cellular GSH levels and significant LDH leakage in rodent SMC cultures. The cytotoxic responses to 0.2-200 μM AAM in secondary cultures of avian SMCs were comparable to those observed in primary culture. In contrast, AAM-induced enzyme leakage did not consistently correlate with changes in GSH content in subcultured rodent SMCs. Challenge with 200 μM acrolein (ACR) for 4 h reduced the GSH content in avian, but not rodent, subcultures of SMCs. However, significant LDH leakage occurred in subcultures of both cell types upon exposure to ACR. Although hydrogen peroxide (H2O2) did not modulate GSH levels in avian or rodent cultures, leakage of LDH was observed in rat SMCs challenged with 200 μM H2O2. Removal of serum did not alter the cytotoxic responses of avian subcultures to 200 μM AAM for 24 h, but fully prevented cytotoxicity in rodent subcultures. These data suggest that potentially significant variations in the sequence of events leading to injury may exist between quail and rat aortic SMCs. These differences may contribute to the enhanced avian susceptibility to AAM-induced aortic injury in vivo.

Original languageEnglish (US)
Pages (from-to)61-76
Number of pages16
JournalJournal of Toxicology and Environmental Health
Volume40
Issue number1
StatePublished - 1993
Externally publishedYes

Fingerprint

Allylamine
Smooth Muscle Myocytes
Muscle
Rodentia
Cells
L-Lactate Dehydrogenase
Acrolein
Rats
Cytotoxicity
Enzymes
Cell Culture Techniques
Coturnix
Quail
Wounds and Injuries
Serum
Cell culture
Hydrogen peroxide
Hydrogen Peroxide
Glutathione

ASJC Scopus subject areas

  • Toxicology
  • Pollution

Cite this

Comparative cytotoxic responses of cultured avian and rodent aortic smooth muscle cells to allylamine. / Ramos, Kenneth; Thurlow, C. H.

In: Journal of Toxicology and Environmental Health, Vol. 40, No. 1, 1993, p. 61-76.

Research output: Contribution to journalArticle

@article{524edd8e1867485cae8c579a88948c69,
title = "Comparative cytotoxic responses of cultured avian and rodent aortic smooth muscle cells to allylamine",
abstract = "The present studies were designed to compare the acute cytotoxic responses of cultured avian and rodent aortic smooth muscle cells (SMCs) to allylamine (AAM), a selective vascular toxin. SMCs were isolated from male Japanese quail or Sprague-Dawley rats and established in culture by standard procedures. Cellular glutathione (GSH) content and lactate dehydrogenase (LDH) leakage were used as indices of cytotoxicity. Exposure of avian and rodent SMCs in primary culture to AAM (0.2-200 μM) for 4 h was associated with a significant reduction in cellular GSH and enzyme leakage in cultures of both cell types. Increased exposure time to 24 h further depleted cellular GSH levels and enhanced the leakage of LDH in primary cultures of avian SMCs. In contrast, enhanced LDH leakage occurred without further GSH depletion in primary cultures of rodent SMCs upon exposure to AAM for 24 h. Removal of serum did not modulate the cytotoxic response profile of primary cultures of avian SMCs treated with 200 μM AAM, but was associated with marked elevation in cellular GSH levels and significant LDH leakage in rodent SMC cultures. The cytotoxic responses to 0.2-200 μM AAM in secondary cultures of avian SMCs were comparable to those observed in primary culture. In contrast, AAM-induced enzyme leakage did not consistently correlate with changes in GSH content in subcultured rodent SMCs. Challenge with 200 μM acrolein (ACR) for 4 h reduced the GSH content in avian, but not rodent, subcultures of SMCs. However, significant LDH leakage occurred in subcultures of both cell types upon exposure to ACR. Although hydrogen peroxide (H2O2) did not modulate GSH levels in avian or rodent cultures, leakage of LDH was observed in rat SMCs challenged with 200 μM H2O2. Removal of serum did not alter the cytotoxic responses of avian subcultures to 200 μM AAM for 24 h, but fully prevented cytotoxicity in rodent subcultures. These data suggest that potentially significant variations in the sequence of events leading to injury may exist between quail and rat aortic SMCs. These differences may contribute to the enhanced avian susceptibility to AAM-induced aortic injury in vivo.",
author = "Kenneth Ramos and Thurlow, {C. H.}",
year = "1993",
language = "English (US)",
volume = "40",
pages = "61--76",
journal = "Journal of Toxicology and Environmental Health",
issn = "0098-4108",
publisher = "Taylor and Francis Ltd.",
number = "1",

}

TY - JOUR

T1 - Comparative cytotoxic responses of cultured avian and rodent aortic smooth muscle cells to allylamine

AU - Ramos, Kenneth

AU - Thurlow, C. H.

PY - 1993

Y1 - 1993

N2 - The present studies were designed to compare the acute cytotoxic responses of cultured avian and rodent aortic smooth muscle cells (SMCs) to allylamine (AAM), a selective vascular toxin. SMCs were isolated from male Japanese quail or Sprague-Dawley rats and established in culture by standard procedures. Cellular glutathione (GSH) content and lactate dehydrogenase (LDH) leakage were used as indices of cytotoxicity. Exposure of avian and rodent SMCs in primary culture to AAM (0.2-200 μM) for 4 h was associated with a significant reduction in cellular GSH and enzyme leakage in cultures of both cell types. Increased exposure time to 24 h further depleted cellular GSH levels and enhanced the leakage of LDH in primary cultures of avian SMCs. In contrast, enhanced LDH leakage occurred without further GSH depletion in primary cultures of rodent SMCs upon exposure to AAM for 24 h. Removal of serum did not modulate the cytotoxic response profile of primary cultures of avian SMCs treated with 200 μM AAM, but was associated with marked elevation in cellular GSH levels and significant LDH leakage in rodent SMC cultures. The cytotoxic responses to 0.2-200 μM AAM in secondary cultures of avian SMCs were comparable to those observed in primary culture. In contrast, AAM-induced enzyme leakage did not consistently correlate with changes in GSH content in subcultured rodent SMCs. Challenge with 200 μM acrolein (ACR) for 4 h reduced the GSH content in avian, but not rodent, subcultures of SMCs. However, significant LDH leakage occurred in subcultures of both cell types upon exposure to ACR. Although hydrogen peroxide (H2O2) did not modulate GSH levels in avian or rodent cultures, leakage of LDH was observed in rat SMCs challenged with 200 μM H2O2. Removal of serum did not alter the cytotoxic responses of avian subcultures to 200 μM AAM for 24 h, but fully prevented cytotoxicity in rodent subcultures. These data suggest that potentially significant variations in the sequence of events leading to injury may exist between quail and rat aortic SMCs. These differences may contribute to the enhanced avian susceptibility to AAM-induced aortic injury in vivo.

AB - The present studies were designed to compare the acute cytotoxic responses of cultured avian and rodent aortic smooth muscle cells (SMCs) to allylamine (AAM), a selective vascular toxin. SMCs were isolated from male Japanese quail or Sprague-Dawley rats and established in culture by standard procedures. Cellular glutathione (GSH) content and lactate dehydrogenase (LDH) leakage were used as indices of cytotoxicity. Exposure of avian and rodent SMCs in primary culture to AAM (0.2-200 μM) for 4 h was associated with a significant reduction in cellular GSH and enzyme leakage in cultures of both cell types. Increased exposure time to 24 h further depleted cellular GSH levels and enhanced the leakage of LDH in primary cultures of avian SMCs. In contrast, enhanced LDH leakage occurred without further GSH depletion in primary cultures of rodent SMCs upon exposure to AAM for 24 h. Removal of serum did not modulate the cytotoxic response profile of primary cultures of avian SMCs treated with 200 μM AAM, but was associated with marked elevation in cellular GSH levels and significant LDH leakage in rodent SMC cultures. The cytotoxic responses to 0.2-200 μM AAM in secondary cultures of avian SMCs were comparable to those observed in primary culture. In contrast, AAM-induced enzyme leakage did not consistently correlate with changes in GSH content in subcultured rodent SMCs. Challenge with 200 μM acrolein (ACR) for 4 h reduced the GSH content in avian, but not rodent, subcultures of SMCs. However, significant LDH leakage occurred in subcultures of both cell types upon exposure to ACR. Although hydrogen peroxide (H2O2) did not modulate GSH levels in avian or rodent cultures, leakage of LDH was observed in rat SMCs challenged with 200 μM H2O2. Removal of serum did not alter the cytotoxic responses of avian subcultures to 200 μM AAM for 24 h, but fully prevented cytotoxicity in rodent subcultures. These data suggest that potentially significant variations in the sequence of events leading to injury may exist between quail and rat aortic SMCs. These differences may contribute to the enhanced avian susceptibility to AAM-induced aortic injury in vivo.

UR - http://www.scopus.com/inward/record.url?scp=0027482602&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0027482602&partnerID=8YFLogxK

M3 - Article

VL - 40

SP - 61

EP - 76

JO - Journal of Toxicology and Environmental Health

JF - Journal of Toxicology and Environmental Health

SN - 0098-4108

IS - 1

ER -