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Effect of Olive Oil–Based Emulsion on Human Lymphocyte and Neutrophil Death
Maria Fernanda Cury-Boaventura, PhD*,
Renata Gorjão, PhD ,
Thaís Martins de Lima, PhD,
Jarlei Fiamoncini, PhD,
Rosângela Pavan Torres, PhD ,
Jorge Mancini-Filho, PhD,
Francisco Garcia Soriano, PhD and
Rui Curi, PhD
From the * Post-Graduate Program in Human Movement
Science, Biological Sciences and Health Center, Cruzeiro do Sul University,
São Paulo, Brazil; and the Department
of Physiology and Biophysics, Institute of Biomedical Sciences,
Pharmaceutical Sciences Faculty, and
Division of Clinical Emergency, Faculty of
Medicine, University of São Paulo, São Paulo, Brazil
Correspondence: Maria Fernanda Cury-Boaventura, Physical Education
Post-Graduate Studies, Biological Sciences and Health Center, Cruzeiro do Sul
University, Rua Galvão Bueno, 868, CEP 01506–000, São
Paulo, SP, Brazil. Electronic mail may be sent to
mafecury{at}icb.usp.br.
Background: The incorporation of lipid emulsions in parenteral
diets is a requirement for energy and essential fatty acid supply to
critically ill patients. The most frequently used IV lipid emulsions (LE) are
composed with long-chain triacylglycerols rich in  -6 polyunsaturated
fatty acids (PUFA) from soybean oil, but these LE promote lymphocyte and
neutrophil death. A new emulsion containing 20% soybean oil and 80% olive oil
rich in -9 monounsaturated fatty acids (MUFA) has been hypothesized not
to cause impairment of immune function. In this study, the toxicity of an
olive oil-based emulsion (OOE) on lymphocytes and neutrophils from healthy
volunteers was investigated. Methods: Twenty volunteers were
recruited and blood was collected before a 6-hour infusion of an OOE,
immediately after infusion, and again 18 hours postinfusion. Lymphocytes and
neutrophils were isolated by gradient density. The cells were studied
immediately after isolation and after 24 hours or 48 hours in culture. The
following determinations were carried out: triacylglycerol levels and fatty
acid composition and levels in plasma, lymphocyte proliferation, production of
reactive oxygen species, and parameters of lymphocyte and neutrophil death
(viability, DNA fragmentation, phosphatidylserine externalization,
mitochondrial depolarization, and neutral lipid accumulation).
Results: OOE decreased lymphocyte proliferation, provoked lymphocyte
necrosis, and had no effect on the proportion of viable neutrophils. The
mechanism of cell death induced by OOE involved neutral lipid accumulation but
had no effect on mitochondrial membrane depolarization. Conclusions:
The OOE given as a single dose of 500 mL induced low toxicity to lymphocytes
from healthy volunteers, probably by necrosis.
Journal of Parenteral and Enteral Nutrition, Vol. 32, No. 1,
81-87 (2008)
DOI: 10.1177/014860710803200181
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G. J. Wanten
Letter to the Editor
JPEN J Parenter Enteral Nutr,
July 1, 2009;
33(4):
450 - 450.
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