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Effects of hyperlipidemia on adaptive responses to repeated zinc exposure
Author(s) -
Dye Janice,
Slade Ralph,
McGee John K,
Jaskot Richard H,
Richards Judy H,
LaGier Adriana J
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.38.4
Subject(s) - hyperlipidemia , oxidative stress , dyslipidemia , medicine , systemic inflammation , endocrinology , cholesterol , inflammation , physiology , chemistry , disease , diabetes mellitus
Exposure of individuals with atherosclerosis/coronary heart disease (CHD) to near‐road air pollution correlates epidemiologically with deleterious health outcome. Cardiotoxicity purportedly involves generation of ROS and activation of local/systemic inflammatory pathways. This study used cholesterol‐fed rabbits with varying degrees of hyperlipidemia [none (N), mild (M), or severe (S)] to determine whether the degree of hyperlipidemia reduced their ability to endure repeated exposure to zinc (Zn, 16 g/kg instilled IT once/wk x 4 wk), a metallic subcomponent of near‐road air pollution. Data revealed that before and after Zn exposure, S‐rabbits had higher blood white cell counts, cholesterol, and LDL levels. After the 4th Zn exposure, S‐rabbits had flattened T waves and increased heart rates. At 24 h, S‐rabbits had changes in serum nitrite. At 48 h, M‐ and S‐rabbits had increased NAG and heterophils in lung lavage fluid, while lung gluthione (GSH) content was decreased. S‐rabbits also had decreased liver GSH; and reductions in liver GSH:GSSG ratios correlated with the degree of hyperlipidemia. Data suggest that health risk related to near‐road air pollution exposure in individuals with CHD involves a complex interplay of dyslipidemia, inflammation, and tissue specific antioxidant deficits that impede adaptation to additional pollutant‐induced oxidative stress. (Does not reflect EPA policy.)