Inderpal Soni

Blood Levels of Organochlorine Pesticide Residues and Risk of Reproductive Tract Cancer Among Women from Jaipur, India

Residues of organochlorine pesticides are integral part of our environment. Because of their strong lipophilic and non-biodegradable nature, organisms at higher trophic levels in the food chain tend to accumulate them. The aim of the present study was to assess the influence of organochlorine pesticides upon the occurrence of reproductive tract cancers in women from Jaipur, India. Blood samples were collected from 150 females. In that group, 100 females suffered from reproductive tract cancers like cervical, uterine, vaginal and ovarian cancers, while the rest did not suffer from cancers or any other major disease and were treated as control group. The collected blood samples were subjected to pesticide extraction and analyzed with the help of gas chromatography. The pesticides detected were benzene hexa chlororide and its isomers, dieldrin, heptachlor, dichloro diphenyl trichloro ethane and its metabolites. The data obtained indicate that the organochlorine pesticide residue levels were significantly higher in all the cancer patients as compared with the control group.

Evaluation of the teratogenic potential of phosphamidon in mice by gavage

Phosphamidon, an organophosphate pesticide, is an established cholinesterase inhibitor. Alteration of tissue and plasma cholinesterase activity at a critical developmental period may influence cellular division and growth sufficiently to produce anatomically or functionally abnormal tissue or organ. The present study was, therefore, undertaken to evaluate the teratogenic potential of phosphamidon in pregnant Swiss albino mice, when administered at different gestational days during the period of organogenesis. The animals were sacrificed on day 18 of gestation for routine teratological examinations. It was observed that phosphamidon was more embryotoxic than teratogenic. Maximum effects were observed when administered on day 7 and day 13. Treatment on day 10 produced little effects. Repeated exposure during the organogenetic phase also produced significant adverse effects. This possibly indicates that phosphamidon is more embryotoxic during the post-implantation period (day 7) and during late organogenesis (day 13) as compared to the early organogenesis period (day 10).

Perinatal toxicity of cyfluthrin in mice: developmental and behavioral effects.

The present study was undertaken to evaluate the teratogenic and behavioral effects of perinatal exposure to cyfluthrin (Synthetic Pyrethroid) on mice offspring. Humans are exposed to this compound as it is widely used in various household insecticide formulations and in public health programmes. Pregnant females were exposed to 16 mg/kg (low dose) and 32 mg/kg (high dose) body weight cyfluthrin daily by oral intubation from gestation day 14 through parturition and lactation up to weaning. On 18th day of gestation, 50% females were euthanized for teratological studies and the remaining were allowed to deliver their pups normally. The fetuses were weighed and observed for gross external malformations and routine teratological examination was done. The neonates were observed for neuromotor reflexes (surface righting, tail hang reflex and pivoting) from day 1 up to day 7 after birth. Movement and exploratory behavior of weanlings were observed using ‘open-field’ and ‘hole-board.’ The fetuses did not show any external malformation. Skeletal aberrations observed included poor ossification of the skull and phalanges and short ribs. Surface righting and pivoting were significantly affected by the high dose. Both doses produced significant changes in the locomotion, exploration, and rearing frequencies in the open-field. The study indicates that cyfluthrin when administered at the above-mentioned doses did not elicit significant teratogenicity but both the doses caused significant difference in behavioral activities.

Neurodevelopmental consequences of gestational and lactational exposure to pyrethroids in rats.

Indiscriminate use of pyrethroids has raised serious health related concerns, especially about their effects on children. The present study was designed to assess the developmental neurotoxicity of two pyrethroids; bifenthrin (BIF) and β‐cyfluthrin (CYF) administered at 1/15 of LD50 in rats. Pregnant females were exposed to the test compounds orally throughout gestation and lactation periods. Neonates were weighed and sexed at birth and were observed for any gross abnormality. Growth, viability and weaning indices were calculated during the lactation period. Exposure to both the compounds did not alter the physical developmental parameters viz. eye opening, pinna detachment, and fur appearance. CYF significantly impaired growth and survivability of pups. Behavioral endpoints assessed in neonates (surface righting, pivoting, and negative geotaxis reflex) as well as adults (motor activity and motor coordination) exhibited marked effect of CYF treatment. Administration of BIF to pregnant dams impaired pivoting in neonates. Decreased locomotion in the open‐field and impaired rota‐rod performance were also witnessed in BIF‐exposed animals. Enhanced oxidative stress was seen in corpus striatum, cerebellum, and hippocampus regions of the brain; reduced catalase, superoxide dismutase, and glutathione peroxidase activities were measured in BIF and CYF treated weanlings. Acetylcholinesterase activity was also found to be lowered following administration of both compounds at PND 21. The present results suggest that exposure to pyrethroids during critical periods of growth can induce long term effects on the behavior of animals.

Evaluation of teratogenic potential of cyfluthrin, a synthetic pyrethroid in Swiss albino mice.

A toxicity study was planned to assess the teratogenic potential of cyfluthrin that is widely used as a household insecticide to control mosquitoes, flies and cockroaches. Pregnant Swiss albino mice of one group were orally administered two doses of the pesticide (16 mg/kg and 32 mg/kg body weight) daily during the organogenetic phase (days 5—14) of gestation. The second group received the same two doses daily during the maturation phase (days 14—18) of gestation. The animals receiving the higher dose exhibited burrowing behaviour, which is a characteristic symptom of pyrethroid poisoning. The autopsies were performed on the 18th day of gestation and routine teratological observations were made. No external malformations occurred in any of the fetus. The higher dose significantly reduced the number of live fetuses, litter size and increased the resorption of embryos when administered during organogenesis, while exposure to the pesticide during the maturation phase did not significantly affect the reproductive parameters. During both the phases, the higher dose reduced the maternal weight gain and the average weight of the fetuses. The fetal anomalies observed were reduced ossification of skull bones, widened cranial sutures, short or absent ribs, hydrocephaly of the ventricles, microphthalmia, anophthalmia, pulmonary edema and subcutaneous edema.

Tartrazine induced neurobiochemical alterations in rat brain sub-regions

Tartrazine is a synthetic lemon yellow azo dye primarily used as a food coloring. The present study aimed to screen the neurobiochemical effects of Tartrazine in Wistar rats after administering the Acceptable Daily Intake (ADI) level. Tartrazine (7.5 mg/kg b.w.) was administered to 21 day old weanling rats through oral gavage once daily for 40 consecutive days. On 41st day, the animals were sacrificed and brain sub regions namely, frontal cortex, corpus striatum, hippocampus and cerebellum were used to determine activities of anti-oxidant enzymes viz. Superoxide Dismutase (SOD), Catalase (CAT), Glutathione-Stransferase (GST), Glutathione Reductase (GR) and Glutathione Peroxidase (GPx) and levels of lipid peroxides using Thio-barbituric Acid Reactive Substance (TBARS) assay. Our investigation showed a significant decrease in SOD and CAT activity, whereas there occurred a decline in GST and GR activity with an increase in GPx activity to counteract the oxidative damage caused by significantly increased levels of lipid peroxides. The possible mechanism of this oxidative damage might be attributed to the production of sulphanilc acid as a metabolite in azofission of tartrazine. It may be concluded that the ADI levels of food azo dyes adversely affect and alter biochemical markers of brain tissue and cause oxidative damage.