THE MODULATORY ROLE OF L-CARNITINE ON INFLAMMATION IN EXPERIMENTALLY-INDUCED TESTICULAR TORSION IN WISTAR RATS

Abstract

Testicular torsion (TT) is a urological emergency that leads to testicular tissue loss due to ischaemic damage. Quick diagnosis and urgent treatment is essential in the management of testicular injury. Reperfusion following torsion leads to generation of reactive oxygen species, inflammatory cytokines and adhesion molecule which are harmful to the testicular environment. The aim of the study was to investigate the modulatory effect of L-carnitine on inflammatory mediators during TT. Forty-five adult male Wistar rats were used for to conduct the experimental. The rats were weighed and randomly divided into three groups comprising of fifteen each group. Five animals from each group i.e. Sham, TT and TT treated with 500mg/kg of L-carnitine were sacrificed on day twenty-two (22), forty-two (42) and sixty-two (62) of the study respectively. At the end of the experiment, blood samples were collected from each of the animals through cardiac puncture and automated haematological analyzer was used to determine the white blood cells. 1.6ml of blood was used to determine Erythrocyte sedimentation rate and serum was harvested to assay TNF-α, Interleukin-1α and Interleukin-1β. The results obtained showed significant decrease (0.90±0.45 3mm/hr) in ESR in the IRI for 22 followed by significant increase (4.00±0.70 3mm/hr) in IRI+L for the same duration when compared with the Sham (2.80±1.11 3mm/hr) treated group. There was also significant decrease (9.50±0.30 ×10 3 µL) in WBCs in TT+L for 62 days when compared with sham for the same period (18:75±75 ×10 3 µL). There was no significant difference in the results obtained for both TNF-α and IL-1α across all the groups but there were significant differences in the TT and TT+L for 42 days, and TT for 62 days when compared with their respective sham treated groups. From our findings, we can conclude that L-carnitine was able to ameliorate the level of inflammation occasioned by TT by lowering the levels of ESR, WBCs and IL-1α which are markers of inflammation.