ABSTRACT
Trichinella infections have been documented globally and have been detected in wild and/or domestic animals except Antarctica. There is paucity of information in the metabolic responses of hosts during Trichinella infections and biomarkers for infection that can be used in the diagnosis of the disease. The current study aimed to apply a non-targeted metabolomic approach to identify Trichinella zimbabwensis biomarkers including metabolic response from sera of infected Sprague-Dawley rats. Fifty-four male Sprague-Dawley rats were randomly assigned into T. zimbabwensis infected group (n = 36) and the non-infected control (n = 18). Results from the study showed that the metabolic signature of T. zimbabwensis infection consists of enriched methyl histidine metabolism, disturbance of the liver urea cycle, impeded TCA cycle, and upregulation of gluconeogenesis metabolism. The observed disturbance in the metabolic pathways was attributed to the effects caused by the parasite during its migration to the muscles resulting in downregulation of amino acids intermediates in the Trichinella-infected animals, and therefore affecting energy production and degradation of biomolecules. It was concluded that T. zimbabwensis infection caused an upregulation of amino acids; pipecolic acid, histidine, and urea, and upregulation of glucose and meso-Erythritol. Moreover, T. zimbabwensis infection caused upregulation of the fatty acids, retinoic acid, and acetic acid. These findings highlight the potential of metabolomics as a novel approach for fundamental investigations of host-pathogen interactions as well as for disease progression and prognosis.
ABSTRACT
The mass specific rates of oxygen consumption (M (O(2)) M(b)(-1)), ammonia excretion (M (NH(4)-N) M(b)(-1)) and carbon dioxide production (M (CO(2)) M(b)(-1)) were measured after 7, 14 and 21 days exposure of adult Potamonautes warreni to a sublethal concentration of 1.0 mg Cu l(-1) (15.75 micromol l(-1)). Under control (non-copper-exposed) conditions M (O(2)) M(b)(-1) was 35.7+/-8.5 micromol kg(-1)min(-1) (mean+/-S.D.), M (NH(4)-N) M(b)(-1) 2.92+/-0.26 micromol kg(-1)min(-1) and M (CO(2)) M(b)(-1) 25.6+/-9.0 micromol kg(-1)min(-1). The oxygen:nitrogen (O:N) ratio and respiratory quotient (RQ) were 24.5+/-3.0 and 0.80+/-0.06, respectively. M (O(2)) M(b)(-1) of copper-exposed crabs showed a significant increase after 7 and 14 days, but decreased significantly by 40% after 21 days. From the increased O:N ratio and RQ below 0.7, it is clear that crabs exposed to 1 mg Cul(-1) metabolize lipids during the entire 21-day exposure period. Free fatty acids in the midgut gland were determined by GC-MS, and showed increases of up to 600% in some C14 to C18 fatty acids. It is proposed that the excess lipids inhibit the pyruvate dehydrogenase complex, leading to the acceleration of the gluco- and glyco-neogenic pathways. Increased glyconeogenesis results in elevated glycogen concentrations in all tissues after 21 days. Experiments on acutely exposed P. warreni show increased incorporation of 14C-labelled lactate into glycogen.
