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. 2019 Mar 7;10:380. doi: 10.3389/fimmu.2019.00380

Table 3.

Kidney tissue concentrations of native and oxidized lipids and vitamin Ea.

Controlb LPS SAA Control LPS SAA
n = 8 n = 8 n = 10 n = 8 n = 8 n = 10
4 weeks after starting SAA-treatment 18 weeks after starting SAA-treatment
[FC] nmol/mg P 1.7 (0.3) 1.6 (0.4) 1.7 (0.3) 1.9 (0.5) 1.9 (0.5) 1.8 (0.6)
[TOH] pmol/mg P 127.8 (30.9) 132.9 (31.7) 125.2 (42.9) 142.2 (60.2) 138.2 (46.1) 154.6 (55.8)
[CeO(O)H] pmol/mg P 4.0 (2.3) 1.9 (0.9) 18.3 (4.7)*# 1.4 (2.0) 2.7 (1.4) 24.4 (17.7)*
[C18:2] nmol/mg P 0.3 (0.02) 0.3 (0.02) 0.3 (0.3) 0.4 (0.2) 0.4 (0.2) 0.5 (0.2)
[C20:4] nmol/mg P 0.9 (0.4) 1.1 (0.6) 1.0 (0.5) 2.1 (2.2) 1.2 (0.4) 1.6 (0.7)
[F2-isoprostanes] pg/mg P 21.2 (4.7) 28.5 (9.6) 66.9 (7.8)*, # 35.3 (7.1) 40.2 (7.1) 51.8 (6.1)*#
a

Mice received normal chow and were administered vehicle, LPS or SAA every 3 days over 14 days by i.p. injection (for details see Materials and Methods). At 4 or 18 weeks after SAA treatment, kidneys were harvested, and the following parameters measured in prepared renal tissue by liquid chromatography or an ELISA kit (F2-isoprostanes). Unesterified cholesterol, FC; α-tocopherol (biologically active vitamin E), α-TOH; cholesteryl linoleate, C18:2; cholesteryl arachidonate, C20:4; combined cholesteryl esters (C18:2 and C20:4), CE; CE-derived lipid hydroperoxides and hydroxides, CeO(O)H.

b

Units of measurement are as indicated. Data represent Means ± (SD); n–as indicated.

*

Different to the control; P < 0.05.

#

Different to the corresponding LPS group; P < 0.05.