Clastogenic effect of pesticides in peripheral lymphocytes of cotton-field workers.

We studied clastogenic effects in peripheral lymphocytes of cotton-field workers who were exposed to different pesticides. All the cells were grown in RPMI 1640 medium for 48 and 72 h. The type of aberrations observed in the exposed group are gaps, breaks, dicentrics, exchanges, rings and polyploidy. The frequency of total chromosomal aberrations increased significantly in male pesticide applicators when compared to controls. A significant decrease in mitotic index was observed in the exposed group as compared to the control group. The 48-h cultures showed high incidence of chromosomal aberrations and low mitotic index when compared to 72-h cultures. The difference in chromosomal aberrations between 48- and 72-h cultures was not significant. 24 out of 26 individuals showed ill health effects such as severe giddiness and nervous disorders.

Reproductive performance in population exposed to pesticides in cotton fields in India.

Data on reproductive histories were collected from 1016 couples in which the males were directly exposed to pesticides. For comparison data were collected from 1020 couples who were not exposed to pesticides and belong to the same socioeconomic group and age range. Statistical analysis revealed a significant decrease in fertile males and a significant increase in abortions among the wives of these exposed males when compared to the control group. The frequency of live births decreased significantly and still births, neonatal deaths, and congenital defects showed a significant increase in the offspring of exposed males when compared to the offspring of control group. Smokers exposed to pesticides showed a higher effect than nonsmokers exposed to pesticides. Eighty percent males in the exposed group showed ill health effects such as severe giddiness, nervous, skin, and eye disorders.

Cytogenetic effects of quinalphos in mice.

The cytogenetic effect of quinalphos was studied in Swiss albino mice using the micronucleus test, bone marrow and germ cell chromosome assays and sperm morphology assay. Quinalphos at 5, 10 and 15 mg/kg body weight was administered orally to mice. Quinalphos induced micronuclei in the bone-marrow cells of mice and also caused a significant increase in chromosomal aberrations in bone-marrow cells (at 10 and 15 mg/kg body weight dose levels) and in germ cells (at all tested doses). A high incidence of abnormal sperms was also observed in mice treated with quinalphos.

Frequency of sister chromatid exchange in peripheral lymphocytes of male pesticide applicators.

In the present study 61 male pesticide applicators who worked in cotton fields and regularly sprayed pesticides such as DDT, BHC, endosulfan, malathion, methyl parathion, phosphamidon, dimethoate, monocrotophos, quinalphos fenvelrate, and cypermethrin were analyzed for sister chromatid exchanges, mitotic index, and cell cycle kinetics in peripheral lymphocytes. Subjects who handled pesticides were non-smokers and teetotalers and the data were compared with the matched control group. Statistical analysis revealed that the frequency of sister chromatid exchanges was significantly higher among the pesticide applicators at all the durations of exposure when compared to controls. Subjects exposed to pesticides also showed cell cycle delay and decrease in mitotic index when compared to the control group.

Cytogeneticity of quinalphos and methyl parathion in human peripheral lymphocytes.

1. Four different concentrations of quinalphos and methyl parathion were tested on human peripheral lymphocytes over different time periods, for the analysis of chromosomal aberrations and sister chromatid exchanges (SCEs). 2. A significant increase in chromosomal aberrations was observed when cells were treated with quinalphos for 48 and 72 h and a significant increase in SCEs was observed at all the concentrations and over all the time periods. 3. Methyl-parathion did not induce chromosomal aberrations but it did induce SCEs significantly over all time periods.

Genotoxic effect of benzene hexachloride in cultured human lymphocytes.

Chromosomal aberrations, sister chromatid exchanges, mitotic index and cell kinetics were observed in human peripheral lymphocytes after treatment with four different concentrations (0.0125, 0.025, 0.05 and 0.1 microgram/ml) of benzene hexachloride (BHC), an organochlorine pesticide. Cells were treated with BHC for 24, 48 and 72 h. There was a dose-dependent increase in the frequency of chromosomal aberrations and sister chromatid exchanges. A significant decrease in mitotic index was observed at all concentrations and times of exposure. BHC did not show a significant effect on cell kinetics.

Chromosomal aberrations in peripheral lymphocytes of cotton field workers exposed to pesticides.

Fifty-two pesticide sprayers in cotton fields were selected for the analysis of chromosomal aberrations in peripheral lymphocytes. Twenty-five samples were collected from healthy males who were not exposed to pesticides. Statistical analysis revealed that there was a significant increase in chromosomal aberrations in the exposed population compared to controls. Total chromosomal aberrations increased irrespective of duration of exposure.

Analysis of sister-chromatid exchanges, cell kinetics and mitotic index in lymphocytes of smoking pesticide sprayers.

Whole blood of 50 smokers who were exposed to pesticides was set up in RPMI 1640 medium, and observed for sister-chromatid exchanges (SCEs), cell kinetics (CK) and mitotic index (MI). As controls, blood samples were collected from 20 non-smokers (control I) and 27 smokers (control II) who were not exposed to pesticides. A significant increase in SCEs was observed as the duration of exposure increased. The frequency of M1 metaphases increased significantly whereas M2 and M3+ metaphases decreased in the exposed group. The mitotic index increased in control II and in the exposed population while it showed a decrease at 11-25 years' exposure.

Frequencies of chromosomal aberrations in smokers exposed to pesticides in cotton fields.

Blood samples were collected from 50 smokers who were exposed to the pesticides DDT, BHC, endosulfan, malathion, methyl parathion, monocrotophos, quinolphos, dimethoate, phosphomidon, cypermethrin and fenvelrate. Samples were also collected from 20 non-smokers (control I) and 27 smokers (control II) who were unexposed to pesticides. Control II showed a significant increase in chromosomal aberrations when compared to control I. There was a significant increase in total chromosomal aberrations in smokers exposed to pesticides when compared to unexposed populations.

Screening of chromosomal aberrations and sister chromatid exchanges in peripheral lymphocytes of vegetable garden workers.

1. Twenty-five male workers occupationally exposed to DDT, BHC malathion, parathion, dimethoate, fenitrothion, urea and gromor were selected as subjects for the analysis of chromosomal aberrations and sister chromatid exchanges (SCE) in peripheral lymphocytes. 2. Blood samples were collected from 30 normal healthy males from the same age group and socioeconomic class for the control. 3. The frequency of chromosomal aberrations and SCEs increased significantly irrespective of the duration of exposure to pesticides, when compared to controls.

Chromosomal abnormalities induced by iodine-125 in mouse germ cells.

Swiss albino male mice were injected intraperitoneally with 0, 185, 370 or 555 kBq (0, 5, 10 or 15 microCi) of iodine-125 (125I). All the animals were killed on the sixtieth day and chromosomal aberrations were screened in spermatocytes at meiotic metaphase I. A significant increase in the percentage of chromosomal aberrations including translocations (0, 1.2, 1.8 and 2.3 per cent translocations in controls, 185, 370 and 555 kBq groups respectively) was recorded at all dose levels indicating the clastogenic effects of 125I in mouse spermatocytes.

Iodine-125 induced micronuclei and sperm head abnormalities in mice.

Swiss albino mice were injected with 0 (controls) 5, 10 or 15 microCi of iodine-125 (125I) and a high incidence of micronuclei in young bone marrow erythrocytes and of sperm head abnormalities was observed. The percentage of polychromatic erythrocytes containing micronuclei in mice treated with 0, 2.5, 5 and 7.5 microCi of 125I administered twice (at 30 and 6 h before sampling) was 0.23, 0.44, 0.56 and 0.72, respectively. The percentage (mean) of abnormal sperm recorded in controls during 1-3, 4-5 and 6-8 weeks was 3.3, 3.7 and 3.7 respectively, whereas the values for the same periods in the 5 microCi (5.5, 6.4 and 7.3), 10 microCi (7.7, 8.4 and 10.0) and 15 microCi (10.3, 9.9 and 10.2) groups were significantly higher. These results suggest that 125I can induce genetic damage in both somatic and germ cells.

Dominant lethal induction and testicular uptake of iodine-125 in mice.

The mutagenic potential of 125I was studied using dominant lethal (DL) and testicular uptake studies. Dominant lethality (DL) represents embryonic death resulting from the chromosomal breakage in gametes of parents. When compared to controls, mice treated with different doses of 125I showed significant levels of induced DL. Significant pre-implantation losses were observed and variations in live implantations indicated total losses by the isotope. Dead implantations per pregnant female in the isotope treated groups showed a significant increase from controls indicating induced levels of post-implantation losses. All the stages of spermatogenesis, i.e., spermatozoa, spermatid, spermatocyte and spermatogonia were found to be sensitive to the induction of post-implantation losses, the spermatid stage being the most sensitive. Testicular uptake was measured from 1/2 hour to 72 hours after injection and maximum uptake was recorded at 1/2 hour, indicating the permeability of the blood/testis barrier.

Girls with muscular dystrophy.

Clinical and genetic studies were made on progressive muscular dystrophy in eight young girls. No chromosomal abnormality was observed in these patients and their mothers. The pedigrees of six cases suggested an autosomal recessive inheritance and clinical features were identical with those of Duchenne muscular dystrophy. Two other cases were compatible with childhood muscular dystrophy with autosomal recessive inheritance.

X-linked Duchenne muscular dystrophy in an unusual family with manifesting carriers.

We report a unique case of a 46-year-old female who had signs of Duchenne-like muscular dystrophy on clinical, electromyographic, and laboratory investigation. A brother, sister, maternal uncle, and her own son also had Duchenne type muscular dystrophy. Karyotype analysis in the proband showed both the X chromosomes to be morphologically normal. We discuss different hypothetical mechanisms to account for the family pedigree.