Use this URL to cite or link to this record in EThOS: http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.629404
Title: Lactation and oxidative stress in small mammals
Author: Al Jothery, Aqeel Handil Tarish
ISNI:       0000 0004 5348 7801
Awarding Body: University of Aberdeen
Current Institution: University of Aberdeen
Date of Award: 2014
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Abstract:
During peak lactation female mammals reach a limit in their maximal sustained energy intake (SusEI). The causes of such limits is disputed. In this thesis, I examined the causes of the limits on SusEI at peak lactation, and then explored the consequences of such limits for reproductive performance. Finally I tested a possible physiological mechanism that may underpin the trade-off between reproduction and somatic protection (the oxidative stress theory). To answer these questions, I studied reproductive performance and oxidative stress in two lines of mice previously selected for high and low food intake (MH and ML, respectively). I found that these mice reached a plateau in their food intake around day 13 of lactation. In support of the heat dissipation limits theory, reproductive performance in the MH mice was significantly higher than that of the ML mice. Oxidative damage is expected to be higher among lactating individuals. Moreover, lactating mice with greater reproductive performance are also predicted to experience more oxidative damage. By measuring multiple-markers of oxidative damage and protection in different tissues, I found that lactation resulted in reduced oxidative damage in both brain and serum. Additionally, it did not increase oxidative damage to proteins and DNA in liver. Moreover, multiple measures of oxidative stress in the mammary gland were not significantly different between mice with different reproductive effort. Furthermore, I found that lactating mice with greater reproductive performance (litter size and litter mass) had reduced protein damage in their livers and upregulated protection (HSP70) in their brains. These results were inconsistent with the oxidative stress theory. Finally, I employed a novel approach to assess oxidative stress differences with metabolomics analysis. I found that lactation resulted in significant differences in the metabolome. By focusing on the metabolites that are related to vi oxidative stress, I found that most of these metabolites measured in livers and brains were not affected by lactation which provides more evidence against the oxidative stress theory. My results provide support for the heat dissipation theory as a mechanism explaining the limits on reproductive performance. Moreover it provides comprehensive information against oxidative stress as a mediator of life history trade-offs.
Supervisor: Not available Sponsor: Iraqi Government
Qualification Name: Thesis (Ph.D.) Qualification Level: Doctoral
EThOS ID: uk.bl.ethos.629404  DOI: Not available
Keywords: Laboratory animals ; Lactation ; Oxidative stress
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