The testis is an immunologically privileged organ. Sertoli cells can form a blood-testis barrier and protect sperm cells from self-immune system attacks. Spermatogenesis may be inhibited by severe illness,
bacterial infections and chronic inflammatory diseases but the mechanism(s) is poorly understood. Our objective is to help in understanding such mechanism(s) to develop
protective agents against temporary or permanent testicular dysfunction. Lipopolysaccaride (LPS) is used as a model of animal
sepsis while
L-carnitine (LCR) is used as a
protective agent. A total of 60 male Swiss albino rats were divided into four groups (15/group). The control group received Saline; the 2(nd) group was given LCR (500 mg/kg i.p, once). The third group was treated with LPS (5 mg/kg i.p once) and the fourth group received LCR then LPS after three hours. From each group, five rats were used for histopathological examination. Biochemical parameters were assessed in the remaining ten rats. At the end of the experiment, animals were lightly anaesthetized with
ether where blood samples were collected and testes were dissected on
ice. Sperm count and motility were evaluated from cauda epididymis in each animal. Also, oxidative stress was evaluated by measuring testicular contents of
reduced glutathione (GSH),
malondialdehyde (MDA) and
8-hydroxydeoxyguanosine (8-HDG, the
DNA adduct for oxidative damage) in testicular
DNA. The pro-inflammatory mediator
nitric oxide (NO) in addition to
lactate dehydrogenase (LDHx)
isoenzyme-x activity as an
indicator for normal spermatozoal metabolism were assessed in testicular homogenate. Serum interlukin (IL)-2 level was also assessed as a marker for T-helper cell function. The obtained data revealed that LPS induced marked reductions in sperm's count and motility, obstruction in seminiferous tubules, hypospermia and dilated congested blood vessels in testicular sections concomitant with decreased testicular GSH content and LDHx activity. Moreover, the testicular levels of MDA, 8-HDG (in testicular
DNA) and NO as well as serum
IL-2 level were increased. Administration of LCR before LPS returned both sperm count and motility to normal levels. Also, contents of testicular GSH, MDA, 8-HDG and NO returned back to the corresponding control values. In addition, serum
IL-2 level as well as histological abnormalities were markedly improved in LCR + LPS-treated rats. In conclusion, LPS increased proinflammatory and oxidative stress markers in the testis leading to a marked testicular dysfunction.
L-carnitine administration ameliorates these effects by
antioxidant and/or anti-inflammatory mechanisms suggesting a protective role against
male infertility in severely infected or septic patients.