ABSTRACTS -PESTICIDES AND HORMONES

[Guest guest]

FROM: DONNA M. REILLY

Environ Health Perspect 2001 Dec;109(12):1197-1206

Cognitive Effects of Endocrine-Disrupting Chemicals in Animals.

Schantz SL, Widholm JJ.

Department of Veterinary Biosciences and Neuroscience Program, University of

Illinois at Urbana-Champaign, Urbana, Illinois, USA.

A large number of chemical pollutants including phthalates, alkylphenolic

compounds, polychlorinated biphenyls and polychlorinated dibenzodioxins,

organochlorine pesticides, bisphenol A, and metals including lead, mercury,

and cadmium have the ability to disrupt endocrine function in animals. Some

of these same chemicals have been shown to alter cognitive function in

animals and humans. Because hormonally mediated events play a central role in

central nervous system development and function, a number of researchers have

speculated that the changes in cognitive function are mediated by the

endocrine-like actions of these chemicals. In this paper we review the

evidence that cognitive effects of chemicals classified as environmental

endocrine disruptors are mediated by changes in hormonal function. We begin

by briefly reviewing the role of gonadal steroids, thyroid hormones, and gluc

ocorticoids in brain development and brain function. We then review the

endocrine changes and cognitive effects that have been reported for selected

endocrine-disrupting chemicals, discuss the evidence for causal relationships

between endocrine disruption and cognitive effects, and suggest directions

for future research.

PMID: 11748026 [PubMed - as supplied by publisher]

-------------------------------------------------------------------------

1: Drug Chem Toxicol 2001 Nov;24(4):359-420

Incorporation of endocrine disruption into chemical hazard scoring for

pollution prevention and current list of endocrine disrupting chemicals.

Whaley DA, Keyes D, Khorrami B.

West Virginia University (WVU), Industrial and Management Systems Engineering

Dept., Room 321, Mineral Resources Building, town, WV 26506, USA.

Research continues to support the theory of endocrine disruption. Endocrine

disruption is defined as the ability of a chemical contaminating the

workplace or the environment to interfere with homeostasis, development,

reproduction, and/or behavior in a living organism or it's offspring. Certain

classes of environmentally persistent chemicals such as polychlorinated

biphenyls (PCBs), dioxins, furans, and some pesticides can adversely effect

the endocrine systems of aquatic life and terrestrial wildlife. The

University of Tennessee, Knoxville (UTN), developed a method for hazard

scoring chemicals for the aquatic ecosystem. The Indiana Clean Manufacturing

Technology and Safe Materials Institute at Purdue University (CMTI) later

expanded the scoring system to include terms for worker hazard as well as

terms for contamination of soil and air quality, and for stratospheric ozone

depletion. We call the CMTI chemical hazard score the Purdue score. At West

Virginia University, two improvements of the Purdue chemical hazard score are

developed, a normalizing of the term for soil contamination, and addition of

hazard score terms for ecosystem endocrine disruption. The results of

incorporating endocrine disruption terms into the hazard scoring equations

resulted in increased hazard rankings, often substantially increased, for 26

endocrine disrupting chemicals (EDCs) among 200 Superfund chemicals. Because

data suggesting human endocrine disruption from such chemicals is still

controversial, no endocrine disruptor term has been added to the human

toxicity portions of the chemical hazard scoring system at this time. The

third product of this work is assembly of a current consolidated list of (1)

established or probable, mostly synthetic, industrial chemical and medication

EDCs and (2) suspect (less certain) synthetic and natural (phytoestrogen)

possible endocrine disrupting chemicals, with the goal of contributing to

future development of quantitative structure activity relationship software

for predicting whether an untested chemical is likely to be an endocrine

disruptor. We conclude that enough endocrine disrupting chemicals are now

identified to make an attempt at developing structure activity estimates of

disrupting potential worthwhile. Further, we conclude that within a group of

200 chemicals of concern to the US EPA, the addition of endocrine disrupting

terms to the Purdue score substantially increases its representativeness in

reflecting ecological exposure hazard. We have developed this enhanced Purdue

score risk management tool to be of assistance to industry.

PMID: 11665649 [PubMed - in process]

------------------------------------------------------------------------

Endocr Rev 2001 Jun;22(3):319-41

Environmental signaling: what embryos and evolution teach us about endocrine

disrupting chemicals.

McLachlan JA.

Department of Pharmacology, Tulane University Health Sciences Center,

Environmental Endocrinology Laboratory, Center for Bioenvironmental Research,

Tulane and Xavier Universities, New Orleans, Louisiana 70112-2699, USA.

john.mclachlan@...

The term " endocrine disrupting chemicals " is commonly used to describe

environmental agents that alter the endocrine system. Laboratories working in

this emerging field-environmental endocrine research-have looked at chemicals

that mimic or block endogenous vertebrate steroid hormones by interacting

with the hormone's receptor. Environmental chemicals known to do this do so

most often with receptors derived from the steroid/thyroid/retinoid gene

family. They include ubiquitous and persistent organochlorines, as well as

plasticizers, pharmaceuticals, and natural hormones. These chemicals function

as estrogens, antiestrogens, and antiandrogens but have few, if any,

structural similarities. Therefore, receptor-based or functional assays have

the best chance of detecting putative biological activity of environmental

chemicals. Three nuclear estrogen receptor forms-alpha, beta, and gamma-as

well as multiple membrane forms and a possible mitochondrial form have been

reported, suggesting a previously unknown diversity of signaling pathways

available to estrogenic chemicals. Examples of environmental or ambient

estrogenization occur in laboratory experiments, zoo animals, domestic

animals, wildlife, and humans. Environmentally estrogenized phenotypes may

differ depending upon the time of exposure-i.e., whether the exposure

occurred at a developmental (organizational and irreversible) or

postdevelopmental (activational and reversible) stage. The term " estrogen "

must be defined in each case, since steroidal estrogens differ among

themselves and from synthetic or plant-derived chemicals. An " estrogen-like

function " seems to be an evolutionarily ancient signal that has been retained

in a number of chemicals, some of which are vertebrate hormones. Signaling,

required for symbiosis between plants and bacteria, may be viewed, therefore,

as an early example of hormone cross-talk. Developmental feminization at the

structural or functional level is an emerging theme in species exposed,

during embryonic or fetal life, to estrogenic compounds. Human experience as

well as studies in experimental animals with the potent estrogen

diethylstilbestrol provide informative models. Advances in the molecular

genetics of sex differentiation in vertebrates facilitate mechanistic

understanding. Experiments addressing the concept of gene imprinting or

induction of epigenetic memory by estrogen or other hormones suggest a link

to persistent, heritable phenotypic changes seen after developmental

estrogenization, independent of mutagenesis. Environmental endocrine science

provides a new context in which to examine the informational content of

ecosystem-wide communication networks. As common features come to light, this

research may allow us to predict environmentally induced alterations in

internal signaling systems of vertebrates and some invertebrates and

eventually to explicate environmental contributions to human reproductive and

developmental health.

Publication Types:

* Review

* Review, Tutorial

PMID: 11399747 [PubMed - indexed for MEDLINE]

------------------------------------------------------------------------

Environ Health Perspect 2001 Dec;109(12):1237-1240

Organophosphorous Pesticide Exposure Increases the Frequency of Sperm Sex

Null Aneuploidy.

Recio R, Robbins WA, Borja-Aburto V, Moran-ez J, Froines JR,

RM, Cebrian ME.

Seccion de Toxicologia, Centro de Investigacion y de Estudios Avanzados del

IPN (CINVESTAV), Mexico DF, Mexico; Departamento de Biologia de la

Reproducion, Centro de Investigacion Biomedica, Facultad de Medicina de

Torreon, Universidad Autonoma de Coahuila, Torreon, Coahuila, Mexico.

It has been estimated that 4 of 1,000 live births and 35% of spontaneous

abortions are aneuploid and that an important proportion of embryo and

newborn aneuploidy is of paternal origin. Exposure to organophosphorous

pesticides (OP) has been associated with sperm hyperploidy/polyploidy.

Therefore, we aimed to assess the frequency of sperm aneuploidy (X, Y, and

18) and its relationship with urinary OP metabolites in agricultural workers.

We performed multicolor fluorescence in situ hybridization on samples from

nine men obtained before and during the pesticide spraying season to assess

sperm aneuploidy. We measured urinary OP metabolite levels by gas-liquid

chromatography. Aneuploidies were found in 0.67% of total sperm nuclei. The

most frequent aneuploidy was the lack of a sexual chromosome or sex null

(0.19%), followed by XY18 (0.15%) and XY18-18 (0.06%). OP metabolites

detected at higher concentrations were dimethylthiophosphate,

dimethyldithiophosphate, and diethylphosphate (DEP). There were no

differences in average aneuploidy frequency or urinary metabolite levels

between samples collected before and after exposure. However, Poisson

regression analysis adjusted for age, alcohol intake, and sperm concentration

showed significant associations between OP metabolite concentrations and

increased frequency of sperm aneuploidies. The association was more evident

between DEP and sex null, and the risk increased further during the spraying

season. Thus, OP exposure could interfere with sperm chromosome segregation

and increase the risk for genetic syndromes, such as 's. Further

studies are required to assess the prevalence of spontaneous abortions, birth

defects, and genetic syndromes in agricultural communities.

PMID: 11748030 [PubMed - as supplied by publisher]

------------------------------------------------------------------------

1: Environ Health Perspect 2001 Dec;109(12):1291-1299

Prenatal Exposure of the Northern Quebec Inuit Infants to Environmental

Contaminants.

Muckle G, Ayotte P, Dewailly E E, son SW, son JL.

Department of Social and Preventive Medicine, Laval University and Public

Health Research Unit, CHUQ Research Center (CHUL), Beauport, Quebec, Canada.

The Inuit population residing in Nunavik (northern Quebec, Canada) relies on

species from the marine food web for subsistence and is therefore exposed to

high doses of environmental contaminants such as polychlorinated biphenyls

and methylmercury and to a lesser extent lead. In view of the neurotoxic

properties of these substances following developmental exposure, we initiated

a study on infant development in this remote coastal population. Here we

report the magnitude of prenatal exposure to these contaminants and to

selective nutrients in Inuit mothers and their newborns who were recruited on

the Hudson Bay coast. We conducted interviews during the women's pregnancies

and at 1 and 11 months postpartum and collected biological samples for

mercury, lead, polychlorinated biphenyls (PCBs), and chlorinated pesticides

analyses as well as selenium and N-3 polyunsaturated fatty acids (n3-PUFA).

Cord blood, maternal blood, and maternal hair mercury concentrations averaged

18.5 & mgr;g/L, 10.4 & mgr;g/L, and 3.7 & mgr;g/g, respectively, and are similar

to those found in the Faroe Islands but lower than those documented in the

Seychelles Islands and New Zealand cohorts. Concentrations of PCB congener

153 averaged 86.9, 105.3, and 131.6 & mgr;g/kg (lipids) in cord plasma,

maternal plasma, and maternal milk, respectively; prenatal exposure to PCBs

in the Nunavik cohort is similar to that reported in the Dutch but much lower

than those in other Arctic cohorts. Levels of n3-PUFA in plasma phospholipids

and selenium in blood are relatively high. The relatively low correlations

observed between organochlorine and methylmercury concentrations may make it

easier to identify the specific developmental deficits attributable to each

toxicant. Similarly, the weak correlations noted between environmental

contaminants and nutrients will facilitate the documentation of possible

protective effects afforded by either n3-PUFA or selenium against neurotoxic

contaminants.

PMID: 11748038 [PubMed - as supplied by publisher]

------------------------------------------------------------------------

NO ABSTRACT AVAILABLE YET

Bull Environ Contam Toxicol 2002 Jan;68(1):72-8

Pesticides and polychlorinated biphenyl residues in human adipose tissue.

ttini M, Guerranti C, Aurigi S, Corsi I, Focardi S.

Department of Environmental Sciences, University of Siena, Via delle Cerchia

3, 53100 Siena, Italy.

PMID: 11731834 [PubMed - in process]

Food Chem Toxicol 2002 Jan;40(1):33-41 Related Articles, LinkOut, Books

Degradation of organochlorine pesticides by meat starter in liquid media and

fermented sausage.

Abou-Arab AA.

Dairy and Food Technology Department, National Research Center, Dokki, Cairo,

Egypt

The effect of meat starter on the degradation of DDT and lindane was

investigated. The insignificant role of Lactobacillus plantarum in degrading

p,p'-DDT and lindane presented in tryptone soya broth (TSB) and mineral salt

medium (MSM) with or without 120 ppm nitrite was observed.The degradation of

DDT and lindane by Micrococcus varians in TSB and MSM with or without nitrite

were studied. The results indicated that DDT or lindane were degraded during

the incubation period. The reduction in DDT at the end of the incubation

period (15 days) was about 24.1 and 32.5% in TSB and MSM without nitrite,

respectively. Corresponding values in the same media with nitrite were 37.5

and 46.4%. Regarding the reduction in lindane, it was recorded as 27.9 and

40.0% in TSB and MSM without nitrite, respectively and 38.4 and 48.4% in the

same media with nitrite. The results indicated that culture media M. varians

metabolized DDT mainly to DDD and lindane mainly to 2,4-, 2,5-, 2,6- and

3,4-dichlorophenol; 2,3,4- and 2,3,5-trichlorophenol; hexachlorobenzene; and

pentachlorophenol. The effect of pesticides on the growth rate of meat

starter was also investigated. The addition of DDT or lindane resulted in a

slight decrease in counts of the strains during the initial incubation in TSB

or MSM. Then the microorganisms recovered and began to grow logarithmically,

but not as well as in a normal situation. The effect of fermentation stage by

meat starter on DDT and lindane in fermented sausage was recorded. The

results indicated that during the 72 h of fermentation, the reduction was 10

and 18% of DDT and lindane, respectively. These results confirmed that the

fermentation process in meat products reduced pesticide residues and these

reductions were due to the activity of meat starter.

PMID: 11731034 [PubMed - in process]

------------------------------------------------------------------------

1: Environ Health Perspect 2000 Jun;108 Suppl 3:433-8

Thyroidal dysfunction and environmental chemicals--potential impact on brain

development.

Porterfield SP.

Medical College of Georgia, Augusta, Georgia, USA. sporterf@...

Certain polyhalogenated aromatic hydrocarbons such as polychlorinated

biphenyls (PCBs) and dibenzo-p-dioxins (dioxins, 2,3,7,

8-tetrachlorodibenzo-p-dioxin) have been shown to have neurotoxic effects and

to alter thyroid function during critical periods of thyroid

hormone-dependent brain development. This has led to the suggestion that some

of the neurotoxic effects of these compounds could be mediated through the

thyroid system. Thyroid hormones are essential for normal brain development

during a critical period beginning in utero and extending through the first 2

years postpartum. They regulate neuronal proliferation, migration, and

differentiation in discrete regions of the brain during definitive time

periods. Even transient disruption of this normal pattern can impair brain

development. Thyroid hormones are necessary for normal cytoskeletal assembly

and stability and the cytoskeletal system is essential for migration and

neuronal outgrowth. In addition, they regulate development of cholinergic and

dopaminergic systems serving the cerebral cortex and hippocampus. Animals

perinatally exposed to certain environmental organohalogens such as many of

the PCBs and dioxins have abnormal thyroid function and neurologic

impairment. Although there are both species and congener variabilities, most

reports show exposure results in thyroid enlargement and reduced serum T(4)

levels with normal T(3) levels. Initial research concentrated on studying the

direct actions of xenobiotics on the thyroid; however, some of these

compounds bear a structural resemblance to the natural thyroid hormones and

have high affinity with thyroid hormone-binding proteins such as

transthyretin. These compounds could act as agonists or antagonists for

receptors of the thyroid/steroid/retinoic acid superfamily. These

structurally similar organohalogens could act at multiple points to alter

thyroid hormone action. The similarity of the neurologic impairment seen in

thyroid disorders to that seen following PCB or dioxin exposure suggests that

one mechanism of neurotoxicity of these compounds could involve interaction

with the thyroid system.

PMID: 10852841 [PubMed - indexed for MEDLINE]

------------------------------------------------------------------------

Nature 2001 Sep 13;413(6852):128-9

Nitrogen fixation. Endocrine disrupters and flavonoid signalling.

Fox JE, Starcevic M, Kow KY, Burow ME, McLachlan JA.

Environmental Endocrinology Laboratory, Center for Bioenvironmental Research

at Tulane and Xavier Universities, New Orleans, Louisiana 70112, USA.

Nitrogen fixation is a symbiotic process initiated by chemical signals from

legumes that are recognized by soil bacteria. Here we show that some

endocrine-disrupting chemicals (EDCs), so called because of their effect on

hormone-signalling pathways in animal cells, also interfere with the

symbiotic signalling that leads to nitrogen fixation. Our results raise the

possibility that these phytochemically activated pathways may have features

in common with hormonal signalling in vertebrates, thereby extending the

biological and ecological impact of EDCs.

PMID: 11557969 [PubMed - indexed for MEDLINE]

------------------------------------------------------------------------

Horm Behav 2001 Sep;40(2):234-47

Neuroendocrine and behavioral implications of endocrine disrupting chemicals

in quail.

Ottinger MA, Abdelnabi MA, Henry P, Mc S, N, Wu JM.

Department of Animal and Avian Sciences, University of land, College

Park, land, 20706

Studies in our laboratory have focused on endocrine, neuroendocrine, and

behavioral components of reproduction in the Japanese quail. These studies

considered various stages in the life cycle, including embryonic development,

sexual maturation, adult reproductive function, and aging. A major focus of

our research has been the role of neuroendocrine systems that appear to

synchronize both endocrine and behavioral responses. These studies provide

the basis for our more recent research on the impact of endocrine disrupting

chemicals (EDCs) on reproductive function in the Japanese quail. These

endocrine active chemicals include pesticides, herbicides, industrial

products, and plant phytoestrogens. Many of these chemicals appear to mimic

vertebrate steroids, often by interacting with steroid receptors. However,

most EDCs have relatively weak biological activity compared to native steroid

hormones. Therefore, it becomes important to understand the mode and

mechanism of action of classes of these chemicals and sensitive stages in the

life history of various species. Precocial birds, such as the Japanese quail,

are likely to be sensitive to EDC effects during embryonic development,

because sexual differentiation occurs during this period. Accordingly, adult

quail may be less impacted by EDC exposure. Because there are a great many

data available on normal development and reproductive function in this

species, the Japanese quail provides an excellent model for examining the

effects of EDCs. Thus, we have begun studies using a Japanese quail model

system to study the effects of EDCs on reproductive endocrine and behavioral

responses. In this review, we have two goals: first, to provide a summary of

reproductive development and sexual differentiation in intact Japanese quail

embryos, including ontogenetic patterns in steroid hormones in the embryonic

and maturing quail. Second, we discuss some recent data from experiments in

our laboratory in which EDCs have been tested in Japanese quail. The Japanese

quail provides an excellent avian model for testing EDCs because this species

has well-characterized reproductive endocrine and behavioral responses.

Considerable research has been conducted in quail in which the effects of

embryonic steroid exposure have been studied relative to reproductive

behavior. Moreover, developmental processes have been studied extensively and

include investigations of the reproductive axis, thyroid system, and stress

and immune responses. We have conducted a number of studies, which have

considered long-term neuroendocrine consequences as well as behavioral

responses to steroids. Some of these studies have specifically tested the

effects of embryonic steroid exposure on later reproductive function in a

multigenerational context. A multigenerational exposure provides a basis for

understanding potential exposure scenarios in the field. In addition,

potential routes of exposure to EDCs for avian species are being considered,

as well as differential effects due to stage of the life cycle at exposure to

an EDC. The studies in our laboratory have used both diet and egg injection

as modes of exposure for Japanese quail. In this way, birds were exposed to a

specific dose of an EDC at a selected stage in development by injection.

Alternatively, dietary exposure appears to be a primary route of exposure;

therefore experimental exposure through the diet mimics potential field

situations. Thus, experiments should consider a number of aspects of exposure

when attempting to replicate field exposures to EDCs. Copyright 2001 Academic

Press.

PMID: 11534988 [PubMed - in process]

------------------------------------------------------------------------

Toxicology 2001 Sep 14;166(1-2):79-89

Comparison of an array of in vitro assays for the assessment of the

estrogenic potential of natural and synthetic estrogens, phytoestrogens and

xenoestrogens.

Gutendorf B, Westendorf J.

Department of Toxicology, Medical School, University of Hamburg,

Vogt-Koelln-Strasse 30, D-22527 Hamburg, Germany. gutendorf@...

Many chemicals in surface waters and sediments have recently been discovered

to have estrogenic/antiestrogenic activity. Among these compounds, known as

'endocrine disrupters', are natural and synthetic hormones, phytoestrogenes

and a variety of industrial chemicals, such as certain detergents and

pesticides. " These substances are supposed to affect the development and

reproduction in wildlife and humans " ...... and may also be involved in the

induction of cancer. In order to assess the estrogenic/antiestrogenic

potential of pure compounds and complex environmental samples we compared an

array of in vitro test systems, (i) two luciferase reporter gene assays using

transgenic human MVLN cells (derived from MCF-7 cells) and HGELN cells

(derived from HeLa cells); (ii) a competitive binding assay with recombinant

human estrogen receptors (ER) alpha and beta; and (iii) a proliferation assay

with MCF7-cells (E-Screen). The sensitivity of the assays for

17-beta-estradiol decreased in the order:

MVLN-cells=E-Screen>HGELN-cells>binding to ER-alpha>binding to ER-beta. A

good correlation was obtained between the estrogenic potencies of 11

compounds (17-beta-estradiol (E(2)), estrone (E(1)), estriol (E(3)),

ethinylestradiol (EE(2)), diethylstilbestrol (DES), coumestrol,

beta-sitosterol, genistein, 4-nonylphenol, 4-octylphenol, bisphenol A) in the

three tissue culture assays. The relative potencies of the compounds obtained

by the cell free binding assays were one to two orders of magnitude higher

compared with the cell culture assays. The phytoestrogens showed a preference

to bind to ER-beta, but only genistein showed a much lower activity in the

E-Screen (growth induction in breast cancer cells) compared with the

luciferase induction in MVLN and HGELN-cells.

PMID: 11518614 [PubMed - indexed for MEDLINE]

------------------------------------------------------------------------

Hum Reprod 2001 Aug;16(8):1768-76

Contribution of environmental factors to the risk of male infertility.

Oliva A, Spira A, Multigner L.

Unidad de Andrologia, Hospital Italiano Garibaldi, 2000 rio, Argentina.

BACKGROUND: An increasing number of reports suggest that chemical and

physical agents in the environment, introduced and spread by human activity,

may affect male fertility in humans. We investigated the relationships

between exposure to environmental agents and seminal characteristics, and the

concentrations of reproductive hormones in the serum of men seeking

infertility treatment. METHODS: We studied 225 male partners from

consecutively recruited couples, who had their first infertility consultation

between 1995 and 1998, in the Litoral Sur region of Argentina, one of the

most productive farming regions in the world. RESULTS: A multivariate

logistic regression model showed that exposure to pesticides and solvents is

significantly associated with sperm threshold values well below the limit for

male fertility. We also found that men exposed to pesticides had higher serum

oestradiol concentrations, and that men exposed to solvents had lower LH

concentrations than non-exposed men. All of these effects were greater in men

with primary infertility than in men with secondary infertility. CONCLUSION:

We have shown that environmental factors contribute to the severity of

infertility, and that this may worsen the effects of pre-existing genetic or

medical risk factors.

PMID: 11473980 [PubMed - indexed for MEDLINE]

------------------------------------------------------------------------

OLD ABSTRACT

1: Arch Androl 1992 Jul-Aug;29(1):65-8

Glutathione therapy for male infertility.

Lenzi A, Lombardo F, Gandini L, Culasso F, Dondero F.

University Laboratory of Seminology & Immunology of Reproduction, University

of Rome La Sapienza, Italy.

Eleven infertile men were treated with glutathione (600 mg/day IM) for 2

months. The patients were suffering from dyspermia associated with various

andrological pathologies. Standard semen and computer analyses of sperm

motility were carried out before treatment and after 30 and 60 days of

therapy. Glutathione exerted significant effect on sperm motility patterns.

Glutathione appears to have a therapeutic effect on some andrological

pathologies causing male infertility.

PMID: 1503526 [PubMed - indexed for MEDLINE]

Ind Health 2001 Jul;39(3):235-43

Induction of gonadal toxicity to female rats after chronic exposure to

mancozeb. (FUNGICIDE-to kill mold)

Baligar PN, Kaliwal BB.

Post-graduate Department of Studies in Zoology, Karnatak University, Dharwad,

India.

Mancozeb, a fungicide of ethylenebisdithiocarbamate group was orally

administered at doses of 500, 600, 700 and 800 mg/kg body weight/day to

normal virgin rats of Wistar strain for 30 days. The vaginal smear and body

weight of the rats were recorded daily and rats were sacrificed on 31st day.

Estrous cycle was effected by showing a significant decrease in the number of

estrous cycle, duration of proestrus, estrus and metestrus with concomitant

significant increase in the duration of diestrus in all the mancozeb treated

groups when compared with controls. There were a significant decrease in the

number of healthy follicles and a significant increase in the number of

atretic follicles in all the mancozeb treated groups when compared with

controls. The histologic observation of the ovary revealed the presence of

less number of corpora lutea and the size of the ovary was also reduced in

high doses of mancozeb treated rats. There was a significant increase in the

thyroid weight in all the mancozeb treated rats except in 500 mg/kg/d. In

rats treated with 500 mg/kg/d showed a significant increase in the level of

total lipids in the liver. In rats treated with 600 mg/kg/d mancozeb showed a

significant decrease in the levels of glycogen and total lipids in the uterus

and total lipids in the liver. In rats treated with 700 mg/kg/d showed a

significant decrease in the levels of protein in ovary, glycogen, total

lipids, phospholipids and neutral lipids in the uterus and a significant

increase in the levels of phospholipids, neutral lipids in the ovary and

total lipids, phospholipids and neutral lipids in the liver. In rats treated

with 800 mg/kg/d showed a significant decrease in the levels of protein and

glycogen in the ovary and protein, glycogen, total lipids, phospholipids and

neutral lipids in the uterus and a significant increase in the levels of

total lipids, phospholipids and neutral lipids in the ovary and liver when

compared with controls. These observed effect of mancozeb on the estrous

cycle, follicles and biochemical constituents may be due to imbalance in the

hormone or toxic effect.

PMID: 11499999 [PubMed - indexed for MEDLINE]

------------------------------------------------------------------------