No abstract

-Rats were orally fed with different doses viz. 9.6, 12 and 15mg/kg/d from GD 0-20 and examined for evidence of fetotoxicity and teratogenecity to evaluate the potential effects of technical chlorpyrifos (97%). Fetotoxic effects were not observed at tested dose levels as evidenced by number of implantations, number of corpora lutea and live fetuses/dam, but significant alterations were noted in percent δ resorption and fetal weight. There were no major malformations, but some minor anomalies such as reduced parietal ossification and absence of phalanges found significant in high dose were not considered as compound-related effects. On the other hand the accumulation of chlorpyrifos residue in dams was more in brain (0.0328 μg/g) than in liver (0.0071 μg/g).The level of residue in fetuses was in the following order : liver (0.0531 μg/g) > brain (0.0364 μg/g) >placenta (0.040 μg/g) > amniotic fluid (0.0010 μg/g). Although, the total residue was higher in fetuses (0.0447 μg/g) than in dams (0.0120 μg/g), the absence of abnormalities in fetal gross morphology, visceral and skeleton suggest that technical chlorpyrifos at tested dose levels is non-teratogenic in rats.

Mancozeb-a fungicide of ethylenebisdithiocarbamate group was orally administered at doses of 500, 1,000 and 1,500 mg/kg body weight/day for 30, 90,180 and 360 days. Signs of toxicity mortality pattern and loss in body weight were observed in dose dependent manner. However, signs of intoxication and mortality pattern were more pronounced till the exposure of 90 days. A significant increase in testes and decrease in epididymis weight were associated with degeneration in seminiferous and epididymal tubules with loss of sperms. The decrease in gonadal acid phosphatase (ACP), succinic dehydrogenase (SDH) and increase in alkaline phosphatase (ALP), lactate dehydrogenase (LDH) activity were observed with increased serum cholesterol. Sialic acid and protein content of testis and epididymis were also decreased in dose dependent manner. The study has thus indicated marked biochemical and pathological changes in gonads of male rats after chronic exposure to mancozeb.

To evaluate the effect of pre- or posttreatment of selenium (6 micromol/kg b.w., single intraperitoneal injection) in mercury intoxication, rats were exposed to mercury (12 micromol/kg b.w., single intraperitoneal injection). Exposure to mercury resulted in induced oxidative stress in liver, kidney, and brain tissues. Marked changes in serum biochemical parameters together with alterations in histopathology and an induction in metallothionein-I and metallothionein-II mRNA expression in the liver and kidney were observed. Pretreatment with selenium to mercury-exposed animals had protective effect on the liver, whereas posttreatment had partial protection on restoration of altered oxidative stress parameters. In the kidney, pretreatment with selenium showed partial protection on restoration of altered biochemical parameters, whereas no protection was observed in posttreatment. The pretreatment with selenium resulted in restoration of mercury-induced metallothionein-I and metallothionein-II mRNA expression, which was completely restored in the liver whereas partial restoration was observed in the kidney. Posttreatment with selenium resulted in further induction in metallothionein-I and metallothionein-II mRNA expression in the liver and kidney. In the brain, selenium showed partial protection on alerted biochemical parameters. Results indicate that pretreatment with selenium is beneficial in comparison to posttreatment in mercury intoxication. Thus, dietary intake of selenium within safe limit may, therefore, enable us in combating any foreseen effects due to mercury exposure.