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of Fe and V increased the lung injury produced by Ni, illustrating the complexity of
the interactions amongst these metals in vivo.
In the companion study to Dreher et al. (
1997
), Kadiiska et al. (
1997
) instilled
Sprague Dawley rats with a lower dose (500
g) of soluble or insoluble preparations
of the ROFA sample, or with a mixture of V(II), Ni(II) and Fe(III) sulfates in con-
centrations approximately equivalent to those in 500
ʼ
g of ROFA. Twenty four (24)
hours after instillation, acute infl ammatory lung damage was ascertained through
examination of cellular and chemical markers in BALF; the production of free radi-
cals was evaluated using electron spin resonance (ESR) in conjunction with
ʼ
-(4-
pyridyl-1-oxide)-N-tert-butylnitrone (4-POBN) spin-trap. Although no p values
were given, Kadiiska et al. (
1997
) reported that the soluble components of ROFA
produced a signifi cant infl ux of neutrophils and proteins indicative of acute infl am-
mation, and signifi cant increases in the formation of free radicals. The authors sug-
gested that V may play the most signifi cant role in the infl ammatory response
produced by ROFA.
Kodavanti et al. (
1998
) instilled Sprague Dawley rats with doses of 0, 0.833, 3.33,
or 8.33 mg/kg of water soluble and acid-extractable fractions of ROFA samples col-
lected from ten locations within the same oil burning power plant (Table
8
); the metals
present were primarily Fe, V and/or Ni. Twenty four hours after instillation, dose-
dependent increases in infl ammatory markers in BALF were observed, with ROFA
samples containing the highest concentrations of water-extractable Fe, V and Ni, or V
and Ni showing statistically signifi cant increases in some markers. In particular, a
signifi cant positive correlation was found between increased BALF protein levels and
the water-extractable Ni content of the ROFA sample. However, the chemilumines-
cence assay indicated that ROFA containing water-extractable V was more potent in
producing oxidative damage than ROFA containing Ni in addition to V and Fe.
Ghio et al. (
1998
) tested the hypothesis that concentrations of the iron transport
and storage proteins lactoferrin and ferritin in rat lung would increase in response to
exposure to ROFA-containing concentrations of Fe, Ni and V. Sprague Dawley rats
were instilled with 500
ʱ
g ROFA, were sacrifi ced at 4, 25, 48 or 96 h post-exposure,
and ferritin, transferrin and lactoferrin concentrations and activity in the lungs deter-
mined. Measurable concentrations of Fe were present in the lungs of both exposed
and un-exposed rats; but Ni and V were only measurable in exposed animals. Ferritin
and lactoferrin concentrations in the lower respiratory tract of ROFA-treated animals
were transiently increased with signs of visible tissue injury, but the respiratory tract
displayed no infl ux of infl ammatory cells. Concentrations of transferrin in BALF
were signifi cantly increased at 4, 24 and 48 h after ROFA exposure as compared to
control animals. The authors suggested that increases in iron-binding and transport-
ing proteins may be related to control of oxidative stress produced by the metals.
Using the same ROFA sample as used by Kadiiska (
1997
) and Dreher (
1997
),
Kodavanti et al. (
2001
) investigated the acute lung toxicity of the ROFA and con-
stituent metals in healthy normotensive Wistar Kyoto (WKY) and spontaneously
hypertensive (SH) rats instilled with either saline, 0.83 or 3.33 mg ROFA/kg, or
1.5
ʼ
mol/kg of either V or Ni sulfates in saline equivalent to a 2-3 mg dose of
ROFA. BALF markers of acute injury and histological changes in the lung were
ʼ
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