Effect of fraction iv portion of &lt;i&gt;Ximenia americana&lt;/i&gt; stem bark on &lt;i&gt;Trypanosoma congolense&lt;/i&gt; - induced serum enzymes changes in rats

Maikai, VA; Maikai, B V O; Kobo, PI

doi:10.4314/bajopas.v8i2.9

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References 21 publications

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“…The oxidative stress that resulted from increased production of free radicals and hydrogen peroxide by T. brucei brucei, macrophages and the host phagocytic system [17] which deplete blood and organs their antioxidant reserves during T. brucei brucei infection, [18,19,51] can result in degenerative changes in organs and tissues which may cause a breakdown in hepatic or endocrine mechanisms controlling the mobilization of carbohydrate for metabolism [9,18,19,20,29,52]. The above facts made some authors to suggest that terminal hypoglycaemia in trypanosomiasis which affects the glycolysis is likely due to tissue/organ breakdown or derangement of endocrine mechanisms controlling the mobilization of carbohydrate reserves than a direct result of massive consumption of glucose by trypanosomes [53,54].…”

Section: Discussionmentioning

confidence: 99%

Trypanosoma brucei brucei induced hypoglycaemia resulted in severe reduction in hexokinase activity in liver, kidney, brain and heart of untreated Trypanosoma brucei brucei infected mice

Ojo¹,

Chinyio²,

Lot³

2021

Magna Sci. Adv. Res. Rev.

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Trypanosoma brucei brucei depends on mammalian host glucose for survival and establishment of infection. The interference with host glucose results in disturbance of pathways for glucose metabolism and their enzymes. Therefore, this study tried to examine the relationship between untreated Trypanosoma brucei brucei infection and the host hexokinase activity in selected organs that depend on glucose for their normal biological and biochemical functions. The mice for this study were grouped into two: control (uninfected) and infected group. Baseline values for PCV, serum glucose and protein; hexokinase activity and protein concentration in the liver, kidney, heart and brain were obtained for each group. The infected group was intraperitoneally inoculation by 1 104 parasites/mice and monitor for the presence of Trypanosoma brucei brucei from the second day post infection. The same parameters were collected again on days 4 and 11 before the death of the infected group. Protein was determined by colorimetric method using Bradford reagent. PCV was analysed using a sysmex haematology analyser while hexokinase activity was measured spectrophotometrically by a coupled reaction with glucose-6-phosphate dehydrogenase at 340 nm. The result of this study showed that untreated Trypanosoma brucei brucei infection resulted in decrease in PCV, serum glucose, hexokinase activity in the liver, kidney, heart and brain but increase in serum protein. In conclusion, untreated Trypanosoma brucei brucei infection resulted in reduction in host liver, kidney, brain and heart hexokinase activity which probably deprived them of the needed energy and may be the cause of early death in untreated trypanosomiasis.

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