Background: Leptospirosis is a zoonotic disease with world-wide distribution, caused by various serovars of Leptospira
interrogans and is presumed to be the most widespread zoonosis. Hematological and biochemical changes associated with
renal and hepatic pathology are commonly observed in leptospirosis. All leptospires are aerobes and therefore might be
expected to generate peroxides during respiration. Enzymatic reduction of H202 by leptospires has been reported by researchers.
The pathogenesis may be related to direct effects of leptospiral compounds or inflammatory response due to oxidative stress.
The present investigation was designed to study the lipid peroxidation and the activity of antioxidant enzymes in rats
experimentally infected with L. interrogans.
Materials, Methods & Results: Fifty four male adult rats (Wistar) specific pathogen free, weighing in average 200 grams were
used. Rats were divided in nine groups, six animals each group, eight infected groups and one as not infected. Inoculation was
performed intraperitoneally (Day 1), using different serovars of L. interrogans distributed by groups: hardjo (group A), wolffi
(group B), grippotyphosa (group C), canicola (group D), Icterohaemorrhagiae (group E), bratislava (group F), pomona (group
G) and butembo (group H). Group I was composed by not-infected rats, serving as the negative control group. On day 15 PI all
animals were anesthetized with isoflurane for blood collection and subsequently decapitated. Liver, spleen, kidney and brain
were collected from all animals. Blood was allocated in tube without anticoagulant for serum acquisition to measurement of
thiobarbituric acid reactive substances (TBARS). Lipid peroxidation (TBARS levels), superoxide dismutase (SOD), catalase
(CAT) and non-protein thiols (NPSH) were measured in the liver, spleen and kidney, and TBARS were also evaluated in serum
and brain. Increased lipid peroxidation was observed in all infected groups when compared to not-infected (P < 0.05); Increase
of TBARS levels were verified in serum of groups F and G; brain of groups E and G; liver and spleen of groups A, B and C; and
in the kidneys of all infected groups compared to Group I. SOD activity was increased (P < 0.05) in liver samples of groups A
and C; and in the kidney samples of groups A to G. Spleen samples did not show statistical differences to SOD activity. We
observed increase in CAT activity (P < 0.05) in liver samples of groups A, B and G, in spleen samples of groups B and E, and
kidney samples of groups A, B, E, F, G and H. NPSH levels increased (P < 0.05) in spleen of groups B, D, E and G, and kidney
samples of groups A, B, C, D and E. Liver samples had no statistical differences between groups in NPSH levels.
Discussion: Based on our results is possible to conclude that the infection by Leptospira interrogans in Wistar rats shows
differences between serovars utilized experimentally. The results may suggest that oxidative damage to tissues along with
other mechanisms might have taken part in the pathogenesis of leptospirosis and further detailed studies at cellular level are
needed to fully understand the pathogenesis and clinical expression of the disease. Kidneys were confirmed as the major host
organ to leptospires, resulting in a great stress oxidative response and presenting a high activity of scavenger enzymes, as well
as potential generation of oxidative stress to other organs and even to the brain.
