Increased lipid peroxidation and ascorbic Acid utilization in testis and epididymis of rats chronically exposed to lead.
The hypothesis has been recently presented that lead may exert its negative effect at least partially through the increase of reactive oxygen species (ROS) level in tissues. However, little is known about the influence of lead intoxication on equilibrium between generation and elimination of ROS in the male reproductive system. Sexually mature male Wistar rats were given ad libitum 1% of aqueous solution of lead acetate (PbAc) for 9 months. Significantly higher lead concentrations were found in blood [median 7.03 (Q25-Q75: 2.99-7.65) versus 0.18 (0.12-0.99) microg dl-1, P < 0.01], caput epididymis [median 5.51 (Q25-Q75: 4.31-7.83) versus 0.51 (0.11-0.80) microg g-1 d.m., P < 0.001], cauda epididymis [median 5.88 (Q25-Q75: 4.06-8.37) versus 0.61 (0.2 - 1.08) microg g-1 d.m., P < 0.001] and testis [median 1.81 (Q25-Q75: 0.94-2.31) versus 0.17 (0.03-0.3) microg g-1 d.m., P < 0.01] of lead-intoxicated rats when compared to the control. The concentration of ascorbyl radical, generated in vitro from L: -ascorbic acid (present in tissues in vivo) was measured by means of Electron Paramagnetic Resonance (EPR) spectroscopy. The EPR signal of ascorbyl radical in caput epididymis, cauda epididymis, testis and liver of lead acetate-treated animals revealed a significant decrease by 53%, 45%, 40% and 69% versus control tissues, respectively. Plasma L: -ascorbic acid content measured by high performance liquid chromatography (HPLC) method and total antioxidant status (TAS) measured by means of spectrophotometry were also significantly lower in the intoxicated versus control animals (28% and 21%, respectively). In the group exposed to lead the concentration of lipid peroxide in homogenates of the reproductive system organs was significantly elevated versus control group. It can be assumed that the lower EPR signal was caused by decreased tissue concentrations of L: -ascorbic acid. The latter may have resulted from consumption of ascorbic acid for scavenging of ROS excess in tissues of animals chronically exposed to lead.
Marchlewicz
Mariola
M
Department of Histology and Embryology, Pomeranian Medical University, Powstańców Wielkopolskich 72, 70-111, Szczecin, Poland. mola@sci.pam.szczecin.pl
Wiszniewska
Barbara
B
Gonet
Bolesław
B
Baranowska-Bosiacka
Irena
I
Safranow
Krzysztof
K
Kolasa
Agnieszka
A
Głabowski
Wojciech
W
Kurzawa
Rafał
R
Jakubowska
Katarzyna
K
Rać
Monika E
ME
D000818:Animals; D001205:Ascorbic Acid / Q000097:blood / Q000378:metabolism*; D002851:Chromatography, High Pressure Liquid; D004578:Electron Spin Resonance Spectroscopy; D004822:Epididymis / Q000187:drug effects / Q000378:metabolism*; D007854:Lead / Q000097:blood / Q000493:pharmacokinetics / Q000494:pharmacology*; D015227:Lipid Peroxidation / Q000187:drug effects*; D008099:Liver / Q000378:metabolism; D008297:Male; D009942:Organometallic Compounds / Q000097:blood / Q000493:pharmacokinetics / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar; D013737:Testis / Q000187:drug effects / Q000378:metabolism*; D014018:Tissue Distribution; D014275:Trigeminal Caudal Nucleus / Q000378:metabolism; D014527:Uric Acid / Q000097:blood
D009942:Organometallic Compounds; D014527:Uric Acid; D007854:Lead; D001205:Ascorbic Acid; C008261:lead acetate