Citation:

Kodavanti, U., S. Snow, P. Phillips, M. Schladweiler, A. Johnstone, A. Ledbetter, C. Miller, A. Henriquez, J. Richards, AND C. Gordon. The influence of maternal high fat diet on ozone-induced lung injury and inflammation in Long Evans male and female rat offspring. Society of Toxicology, Baltimore, MD, March 12 - 16, 2017.

Impact/Purpose:

There is a growing interest in understanding how maternal diet can increase the sensitivity of offspring to environmental exposures. Our data may suggest that maternal HFD exacerbate ozone-induced lung injury/inflammation in adult male offspring.

Description:

There is a growing interest in understanding how maternal diet can increase the sensitivity of offspring to environmental exposures. In this study, we examined the influence of high fat diet (HFD) during puberty, pregnancy and lactation in Long Evans rats on the susceptibility of male and female adult offspring to acute ozone inhalation. F0 female rats began HFD (60% kcal from fat; Teklad-TD.06414) or control diet (CD; 10.5% kcal from fat; Teklad-TD.08806) at post-natal day (PND) 30. Rats were bred on PND 75 and allowed to give birth. F1 litters at PND 6 were culled to 4 males and 4 females wherever possible, and weaned on PND 21. Offspring received respective HFD or CD until PND 35, after which all offspring were switched to CD. At 5-6 months of age, male and female offspring (n=9-10/group) were exposed to filtered air or 0.8 ppm ozone (4h/day) for 2 days. Systemic metabolites, plethysmography, and bronchoalveolar lavage fluid markers of lung injury/inflammation were assessed within 3 hr post-exposure. Maternal obesity failed to induce changes in offspring weight; however, male offspring were heavier than their age-matched female counterparts. In air-exposed animals, no sex or maternal diet-related differences were apparent in indicators of lung injury/inflammation or plethysmography measures; however, circulating triglycerides were 3-4 times higher in female offspring when compared to males regardless of maternal diet. Ozone-induced hyperglycemia and glucose intolerance were markedly enhanced in males but females were less affected; no significant maternal diet influence was observed. No significant ozone effects were observed in circulating cholesterols and triglycerides in any sex or dietary groups. Ozone-induced changes in breathing parameters and lung injury/inflammation occurred in both sexes, however, effects were more pronounced in males than in females. In general, ozone-induced neutrophilic inflammation, pulmonary protein leakage and lung cell injury markers were exacerbated in male offspring from HFD dams when compared to those from CD dams; this maternal diet influence on ozone sensitivity was minimal in females. These data may suggest that maternal HFD exacerbate ozone-induced lung injury/inflammation in adult male offspring. (Does not reflect the US EPA policy).

Record Details: