Several cytotoxic chemical pollutants inducing peroxidative damages are liable to induce kidney failure. Among these pollutants we find heavy metals such as: lead, nickel, cadmium, vanadium and mercury. Lead is one of the most dangerous metals because it is widely spread in the environment, and because it may be a source of several nervous diseases. The aim of this study is to provide evidence concerning the effect of this metal on the renal function and to try to determine a storage corner in the organism which serves as an indicator of a lead intoxication. Lead acetate was administered by oral route in the drinking water to adult rats aged three months at the rate of 0.3% (P1) and 0.6% (P2). Reference rats received distilled water to drink under the same conditions. The treatment continued for 15, 30, 45, 60 and 90 days. The creatinemia, uremia, glycemia and creatinuria are determined by colorimetric techniques. Lead concentration in blood as well as the lead content of the tail are determined by atomic absorption after nitroperchloric mineralization at the liquid stage. The results showed an increase of creatinemia on the 30th day of the experiment for both sexes in (P1 and P2). The same happened for ureamia. The increase of these two parameters would indicate a renal deficiency which is confirmed by a decrease of creatinuria and urinary pH observed mainly on and after the 45th day of the experiment. An increase of the renal relative weight was noticed in P1 and P2 on the 30th day of the treatment. The determination of the concentration of lead in the blood shows that this factor increases among treated subjects in a constant way, independently of the dose and the duration of the treatment. Nevertheless, the rate increase of lead in the tail seems to be dose-dependent. In conclusion, lead administered by oral route causes a renal deficiency to the rat without distinction between males and females. In addition, the tail seems to be a reliable exposure biomarker that demonstrates lead intoxication. The tail seems to be a dosimeter of lead bio-accumulation. It constitutes an endogenous source of lead impregnation. The concentration of lead in the blood is only an indicator of recent exposure.

Impact of lead given in drinking water on the endocrine and exocrine sexual activity in pubescent rats. Determination of an apoptotic process. This study deals with the impact of chronic exposure to lead on male and female fertility in rats. Male and female rats (3 months old) were fed on commercial tablets (SICO, Sfax). For drinking, some rats were given distilled water (T = controls), the other ones were given distilled water enriched with lead acetate, either 3 (P1 group) or 6 mg ml -1 (P2 group), for 15, 30, 45, 60 or 90 days. In male rats, absolute and relative weights of testis, epididym, prostate and seminal vesicles were found to significantly decrease at day 15 in the P2 group and at day 45 in the P1 group. However, at day 60, these absolute and relative weights returned to control values. Lead-induced pathological changes in spermatogenesis were observed at day 15 by histological study: arrest of cell germ maturation, changes in the Sertoli cells, and presence of apoptotic cells revealed by borated toluidine blue in the testis. Presence of lead deposits was observed after histochemical staining using sodium rhodizonate. Serum testosterone level was found to be lowered at day 15 in both (P1) and (P2) groups, to display a peak at day 60, then to return to controls values, in spite of the continuation of the treatment. In female rats, absolute and relative weights of ovary and uterus were found unchanged. The vaginal smears practised in females revealed the oestrus phase in all groups. Exposed females were mated with control males, and fecundity was assessed 15 days later by counting the number of pregnancies and the number of conspectuses per pregnancy. Fertility was found to be reduced in females of P1 and P2 groups as compared to control females (T group). Lead level in blood was found to be poorly correlated with the level of poisoning, whereas lead accumulation in tail was found to be dose-dependent. Therefore, lead accumulation in tail appears as a more reliable biomarker of exposure to lead. In summary, our study shows that chronic exposure to lead causes a double sexual disorder in rats: first, disorder deals with the hormonal function, which is affected at the early stages of poisoning, but is rapidly corrected; second, disorder deals with the genital tract, affecting the testis and the ovary, resulting in a reduced fertility in both P1 and P2 females, in spite of the presence of a normal oestrus. The cytotoxic effect of lead in males seems to be related to an apoptotic process.

RésuméLes gaz d'éc happement des véhicules automobiles constituent une importante source de pollution urbaine. L'objectif de . cette étude est de mettre en évidence, chez le rat, les effets en fonction du temps, d'expositions répétitives aux gaz d'échap-pement d'un moteur à essence, sur la variation de certains biomarqueurs touchant la fonction hormonale sexuelle mâle, la fonction rénale et l'hémogramme. Les résultats montrent une baisse du taux de la testostérone sérique chez les rats exposés aux gaz d'échappement. Cette baisse est à l'origine d'une stérilité masculine déjà démontrée dans notre laboratoire au cours d'un travail antérieur (histologie testiculaire et expériences d'accouplement). Cette stérilité est réversible parce que les rats pollués retrouvent leur activité sexuelle normale deux mois après arrêt du traitement polluant. Une augmentation du taux de monoxyde de carbone sa nguin, ave c acc umulatio n du plomb au nivea u du sang et de la queue est signalée chez ces rats. Les analyses biochimique s montrent que la glycémie, la créatinémie et l'urée sanguine augmentent chez les rats traités. La créatininurie baisse. Ceci témoigne d'une atteinte rénale. Elles montrent de même chez les rats traités, par comparaison aux témoins, une augmentation du nombre des globules rouges, de l'hématocrite, du taux sanguin d'hémoglobine et du VGM, et une baisse de la CGMH. Le monoxyde de carbone et le plomb détectés dans le sang de ces animaux sont à l'origine de ces perturbations hématologiques.En conclusion, nos résultats montrent que les gaz d'échappement d'automobile à essence induisent chez le rat une baisse du taux de testostérone sérique. Le monoxyde de carbone et le plomb présents dans les gaz d'échappement, et détectés au niveau du sang et de la queue des animaux exposés à ces polluants, sont à l'origine de perturbations sexuelles, rénales et hématologiques. * Laboratoire d 'Écophysiologie anima le, Faculté des AbstractThe automotive exhaust gases constitute an important source of urban pollution. The objectiv e of this study is to explore, in the rat, the effects of repetitive exposure to gasoline automotive exhaust gases on the leve l va riatio ns of serum testosterone, blood lead, bone lead, blood carbon monoxide, on the kidney function and blood parameters.200 rats inhaling a mixture of air and automotive exhaust gas (10/1 , v/v) , are distributed in 4 groups treated during 15, 30, 45 and 60 days. They are compared to non treated controls.Our results show a decrease of serum testosterone level. This result is the origin of a masculine sterility already demonstrated in our laboratory. This sterility seems to be reversible because polluted rats regain their sexual activity , 2 months alt er stopping of the pollutant treatment. An increase of the blood carbon monoxide level with a lead accumulation in blood and in the tail is noticed. Biochemical analyses show that glycaemia, urea, and creatininaemia increase in treated animais. The urinary rate of creatinine decreases. These results indicate kidney defici...