Urban Heat Island (UHI) is a phenomenon that significantly affects the environment, the cities' liveability, and the citizens' well-being. This study aims to perform a comparative study of the microclimate and UHI phenomenon of Ahmedabad City using MODIS and Landsat Satellite Datasets. The satellite datasets were utilized to calculate the UTFVI, NDBI, MBI, MNDWI, and NDWaI to study the city's heat islands and land surface characteristics. The study's findings reveal that Ahmedabad has 35.53

Urban heat islands (UHIs), which are formed by biophysical landscape transformations, have significant adverse effects on environmental quality as well as human health, resources, and facilities. Variations in UHI intensity give rise to urban hotspots (UHSs) and cold spots in different parts of the city. This study identifies such hotspots and cold spots in Delhi by classifying the city into zones of different UHI intensities using biophysical landscapes. The data on the selected biophysical landscapes were obtained from satellite images and secondary sources. The impact of different biophysical landscapes on UHI intensity was calculated using the weighted overlay method performed using ArcGIS software. The city of Delhi was thus divided into four zones, based on UHI intensity. It was found that UHSs cover about 45% of the total area and are mostly located in eastern and central Delhi. While built-up areas form the major source landscape, vegetation cover is the major sink landscape as per land surface temperature (LST) and UHI intensity. The findings of this study will help urban planners and policymakers identify UHSs and adopt suitable policies and measures to mitigate UHIs based on the different intensity zones.

This paper presents the identified four satellite towns around Delhi mega city, namely Gurgaon, Ghaziabad and Gautam Budh Nagar included Noida and Greater Noida, which are well populated and connected with urban core Delhi. Furthermore, the population growth and its impact on Land Use Changes of Delhi and its surrounding towns were considered for the study. The rates of growth of these cities were analyzed through census and multi temporal high-resolution satellite data. The decadal growth rate of Delhi and Gurgaon was more than 50 per cent during 1941-81, and 26.83 and 44.25 in 2011. Similarly in Ghaziabad it was more than 60 per cent during 1951-2011 whereas the Gautam Budh Nagar, shows the rapid growth, 237.10, 269.10, 80.80 and 116.70 during 1981-2011. The impact of this growth has shown in the form of land use changes. The built-up land increased by 8.10 km2 per annum in Delhi, 0.92 km2 in Gurgaon, 4.80 km2 in Ghaziabad and 13.03 km2 in Gautam Budh Nagar whereas, the agricultural land, decline by 7.35 km2, 0.86 km2, 5.45 km2 and 11.60 km2 per annum in this cities. The decadal rate of population growth and land use changes is higher in Gautam Budh Nagar, followed by Delhi, Ghaziabad and Gurgaon. The findings of this study would provide insight to the planners and policy makers for the management of urban land in the field of growth related problems of the city regions.

This research is focused on the land use land cover changes and urban expansion in megacity; Delhi, and highlights the major impact of the rapid growth of population and urbanization on the LULC changes for the period of thirty-four years, which need immediate attention.The multi-temporal satellite data and visual interpretation methods were used through Arc GIS Software.The results show that the built-up land has increased by 14.41 km 2 /annum whereas agricultural, waste, barren and scrub land shrink by 9.59 km 2 /annum, 4.29 km 2 /annum respectively, during this period.The built-up area expanded from 298 km 2 to 773.59 km 2 during 1985 to 2018 on the cost of agricultural, waste, barren, and scrub land.The increment of forest 2.92 percent during this period shows a healthy sign.The findings would provide insight to the planners and policy makers; for the management of urban land, and problems related with the growth of city regions.

This paper is focused on a set of three growing cities of India namely Gurgaon, Ranchi and Jaipur, for the analyses of population growth and land use changes of the past four decades. For this purpose the census data and multi temporal satellite data and GIS software used. The decadal growth rates of the population in these cities are 44.25, 23.98 and 53.16 per cent in 2011. The effect of this growth has shown in the form of land use changes. The built-up land has increased by 1.84 km2, 2 km2, 4.5 km2 per annum, whereas agricultural land declined by 1.75 km2, 1.93 km2, and 4.52 km2 per annum in these cities. The findings of land use land cover and it spatial relationship between the changes of different classes are critical for understanding the past patterns and the consequences of urban growth so as to inform future insight to the planners, policy makers, risk management and conservation strategies for growth related problems.

Di(2-ethylhexyl) phthalate (DEHP) is a ubiquitous environmental toxicant found in consumer products that causes ovarian toxicity. Antral follicles are the functional ovarian units and must undergo growth, survival from atresia, and proper regulation of steroidogenesis to ovulate and produce hormones. Previous studies have determined that DEHP inhibits antral follicle growth and decreases estradiol levels in vitro; however, the mechanism by which DEHP elicits these effects is unknown. The present study tested the hypothesis that DEHP directly alters regulators of the cell cycle, apoptosis, and steroidogenesis to inhibit antral follicle functionality. Antral follicles from adult CD-1 mice were cultured with vehicle control or DEHP (1-100 μg/ml) for 24-96 h to establish the temporal effects of DEHP on the follicle. Following 24-96 h of culture, antral follicles were subjected to gene expression analysis, and media were subjected to measurements of hormone levels. DEHP increased the mRNA levels of cyclin D2, cyclin dependent kinase 4, cyclin E1, cyclin A2, and cyclin B1 and decreased the levels of cyclin-dependent kinase inhibitor 1A prior to growth inhibition. Additionally, DEHP increased the mRNA levels of BCL2-associated agonist of cell death, BCL2-associated X protein, BCL2-related ovarian killer protein, B-cell leukemia/lymphoma 2, and Bcl2-like 10, leading to an increase in atresia. Further, DEHP decreased the levels of progesterone, androstenedione, and testosterone prior to the decrease in estradiol levels, with decreased mRNA levels of side-chain cleavage, 17α-hydroxylase-17,20-desmolase, 17β-hydroxysteroid dehydrogenase, and aromatase. Collectively, DEHP directly alters antral follicle functionality by inhibiting growth, inducing atresia, and inhibiting steroidogenesis.

The impact of growth of cities in the change of urban environment especially in the study of land use and land cover change has drawn attention from scholars in the field of urban studies. This research is focused on a set of three growing cities of India, Gurgaon, Ranchi and Jaipur for the analyses of land use/ land cover changes for the periods of 25 years. The results show that the built-up land has increased, whereas the other categories of land have decreased. The findings would provide insight to the planners and policymakers for the management of urban land in the field of growth related problems of the city regions.

Mono-2-ethyhexyl phthalate (MEHP) is a metabolite of a plasticizer found in many consumer products. MEHP inhibits mouse ovarian follicle growth by reducing 17β-estradiol (E2) production. Yet, whether MEHP causes follicle death (atresia) is unclear. We hypothesized that MEHP causes atresia by altering apoptosis gene expression, and that E2 co-treatment blocks these effects. Follicles were exposed to MEHP (0.36-36μM)±E2 for 48-96h to determine the effect of MEHP±E2 on atresia and gene expression. MEHP increased atresia, but this effect was blocked by co-treatment with E2. MEHP increased the expression of the pro-apoptotic gene Aifm1, but decreased that of the pro-apoptotic gene Bok and the anti-apoptotic gene Bcl2l10. E2 interfered with MEHP-induced changes in Aifm1 and Bcl2l10. Our findings suggest that decreased E2 levels are required for MEHP-induced follicle atresia and that Aifm1, Bok, and Bcl2l10 are involved in this process.

Indian cities are growing rapidly and that results in a wide variety of environmental stresses. In this article, an integrated approach that incorporates Satellite Data and GIS techniques in conjunction with socio-economic data has been used to assess urban environmental issues in Jaipur, the capital city of the Indian state of Rajasthan. The issues addressed in this paper include: changes in land use/land cover changes in surface temperatures based on data collected between 2001 and 2009, and the assessment of surface Urban Heat Island (UHI) both in temperature and vegetation. Least clouded day and night scenes of TERRA/MODIS acquired between 2001 and 2008 have been selected to generate Land Surface Temperature (LST) maps. UHI patterns are analyzed in association with urban vegetation cover, built up land, population density, and surface temperature derived from high-resolution satellite data. The results show that the city has been expanding very rapidly towards the South and South-West due to the presence of Aravalli hills in the Northern direction. The study shows that out of the total area, only 13.12 per cent under moderate potential zone and 0.97 per cent under high UHI potential zone, is located close to the walled city in core region.

Methoxychlor (MXC) is an organochlorine pesticide widely used in many countries against various species of insects that attack crops and domestic animals. MXC reduces fertility by increasing atresia (death) of antral follicles in vivo. MXC also induces atresia of antral follicles after 96 h in vitro. The current work tested the hypothesis that MXC induces morphological atresia at early time points (24 and 48 h) by altering pro-apoptotic (Bax, Bok, Casp3, and caspase activity) and anti-apoptotic (Bcl2 and Bcl-xL) factors in the follicles. The results indicate that at 24 h, MXC increased Bcl-xL and Bax mRNA levels and increased the ratio of Bax/Bcl2. At 48-96 h, MXC induced morphological atresia. At 24-96 h, MXC increased caspase activities. These data suggest that MXC may induce atresia by altering Bcl2 factors and inducing caspase activities in antral follicles.

The chlorinated organic pesticide methoxychlor is a proven endocrine disrupting chemical. Methoxychlor is readily metabolized in the body to form polar metabolites. The major metabolic pathway is demethylation of methoxychlor to mono-OH methoxychlor and bis-OH methoxychlor (HPTE). There is no validated analytical method in the literature for the detection and quantification of methoxychlor and its two major metabolites in cell culture medium. Therefore, in the present study, we developed and validated a simple high performance liquid chromatography (HPLC) method with a one-step liquid/liquid extraction procedure to detect and quantify methoxychlor and its metabolites (mono-OH methoxychlor and HPTE) from alpha-minimum essential media that is used for ovarian follicle cell culture studies. The HPLC diode array detection method reported here readily detects methoxychlor and its metabolites (mono-OH methoxychlor and HPTE), with a limit of detection of methoxychlor, mono-OH methoxychlor, and HPTE in culture medium of about 7.8 ng/120 mu L, 4.8 ng/120 mu L,and 10.5 ng/120 mu L,respectively. The mean extraction efficiency values for methoxychlor, mono-OH methoxychlor, and HPTE were 82%, 88%, and 88%, respectively.

This paper has focused on the monitoring of land use land cover over 34 years. The study has based on secondary and satellite data along with statistical techniques as well as limited field verification. Jaipur City is situated in the North West zone of India. Its population has grown from 0.3 million in 1951 to 2.3 million in 2001 and 2.9 million in 2009. The annual average growth rate from 1971 to 2001 has been in the range of 4.1 to 4.7. The growth rate was the highest in the year 1981 but declined sharply by 0.6 per cent in 1991 and in grew again by 0.2 per cent in 2001. The impact of such growth is seen in the change in land use and led to the congestion of walled city. The population growth has major driving forces of land use change. The crop land has shrinked to 1.60 sq km/year, fallow land 2.94 sq km/ year, wasteland 0.59 sq km/year during 19752009, whereas the builtup l and has increased in the rate of 4.46 sq.km/ year or 1.02 per cent/year. Based on the use of multi resolution and multi temporal satellite data of 1975 to 2009, the spatial and temporal changes in the various types of land uses of city are detected and discusses. Urbanization is now a common feature of all third world countries. Primate cities and mega cities are emerging in developing countries. The growth in the population of cities in developing countries has been attributed to various factors which could be summarized in two: natural population increase and ruralurban mi gration. The cities of the third world have especially experienced population growth. Urban growth has been criticized for its inefficient use of land resources and energy and largescale en croachment on agricultural land. These impacts threaten the principle of sustainable development. However, sustainable urban growth management and development planning need to take account of the dynamic process of temporal urban change. The measurement of urban form can provide a more systematic analysis of the relationships between urban form and process (Yeh and Li, 2001). Batty and Longley (1994), classified urban growth as generally organic (or natural) or planned (or artificial) growth. The distinction between the two is multifold and often blurred. Basically, planned growth appears to be more manmade, in that the patterns produced are more regular, reflecting more control over the building process. Most cities and towns provide a blend of both, usually containing elements of the planned against a backcloth of organic growth. Urban growth is a broad and vague concept that can be subdivided into various types such as sprawling or compact, dispersed (scattered) or clustered, continuous or leapfrog, spontaneous or selforganizing, planned or organic. It may comp rise physical growth, population growth, economic growth and environmental change (decline), although there is often a focus on the physical aspect in the domains of remote sensing and GIS. The appearance of a circular

Di (2-ethylhexyl) phthalate (DEHP) is a plasticizer that has been shown to inhibit growth of mouse antral follicles, however, little is known about the mechanisms by which DEHP does so. Oxidative stress has been linked to follicle growth inhibition as well as phthalate-induced toxicity in non-ovarian tissues. Thus, we hypothesized that DEHP causes oxidative stress and that this leads to inhibition of the growth of antral follicles. To test this hypothesis, antral follicles isolated from CD-1 mice (age 31–35days) were cultured with vehicle control (dimethylsulfoxide [DMSO]) or DEHP (1–100μg/ml)±N-acetyl cysteine (NAC, an antioxidant at 0.25–1mM). During culture, follicles were measured daily. At the end of culture, follicles were collected and processed for in vitro reactive oxygen species (ROS) assays to measure the presence of free radicals or for measurement of the expression and activity of various key antioxidant enzymes: Cu/Zn superoxide dismutase (SOD1), glutathione peroxidase (GPX) and catalase (CAT). The results indicate that DEHP inhibits the growth of follicles compared to DMSO control and that NAC (0.25–1mM) blocks the ability of DEHP to inhibit follicle growth. Furthermore, DEHP (10μg/ml) significantly increases ROS levels and reduces the expression and activity of SOD1 compared to DMSO controls, whereas NAC (0.5mM) rescues the effects of DEHP on ROS levels and SOD1. However, the expression and activity of GPX and CAT were not affected by DEHP treatment. Collectively, these data suggest that DEHP inhibits follicle growth by inducing production of ROS and by decreasing the expression and activity of SOD1.

Bisphenol A (BPA) is used as the backbone for plastics and epoxy resins, including various food and beverage containers. BPA has also been detected in 95% of random urine samples and ovarian follicular fluid of adult women. Few studies have investigated the effects of BPA on antral follicles, the main producers of sex steroid hormones and the only follicles capable of ovulation. Thus, this study tested the hypothesis that postnatal BPA exposure inhibits antral follicle growth and steroidogenesis. To test this hypothesis, antral follicles isolated from 32-day-old FVB mice were cultured with vehicle control (dimethyl sulfoxide [DMSO]), BPA (4.4-440 μM), pregnenolone (10 μg/ml), pregnenolone + BPA 44 μM, and pregnenolone + BPA 440 μM. During the culture, follicles were measured for growth daily. After the culture, media was subjected to ELISA for hormones in the estradiol biosynthesis pathway, and follicles were processed for quantitative real-time PCR of steroidogenic enzymes. The results indicate that BPA (440 μM) inhibits follicle growth and that pregnenolone cotreatment was unable to restore/maintain growth. Furthermore, BPA 44 and 440 μM inhibit progesterone, dehydroepiandrosterone, androstenedione, estrone, testosterone, and estradiol production. Pregnenolone cotreatment was able to increase production of pregnenolone, progesterone, and dehydroepiandrosterone and maintain androstenedione and estrone levels in BPA-treated follicles compared with DMSO controls but was unable to protect testosterone or estradiol levels. Furthermore, pregnenolone was unable to protect follicles from BPA-(44-440 μM) induced inhibition of steroidogenic enzymes compared with the DMSO control. Collectively, these data show that BPA targets the estradiol biosynthesis pathway in the ovary.

Environmental toxicants with the potential to alter fetal development of the reproductive system are of major concern to scientists and the general public alike. In particular, the estrogenic plastic monomer bisphenol A (BPA) is a compound of tremendous concern due to its inclusion in many everyday consumer items including baby bottles and canned foods. While some animal studies have indicated exposure to extremely low doses of BPA (less than 50 µg/kg/day) can result in significant alteration of reproductive endpoints, other studies have found no effects of BPA exposure on reproductive system development. To investigate whether low doses of BPA could affect testis morphogenesis in mice, we conducted a gestational exposure study. Pregnant CD-1 dams (n=3 per treatment group) were orally dosed with corn oil vehicle, 50 µg/kg/day BPA, or 0.5 µg/kg/day BPA from embryonic day 10.5 (E10.5) to E17.5. This time period coincides with sex determination and covers subsequent testis cord organization and expansion. A fourth treatment group received 0.05 µg/kg/day of the known ERalpha agonist diethylstilbestrol (DES) to serve as a positive control. Pups were collected via caesarean section at E19.0, shortly before the time of birth. In utero exposure to BPA or DES did not significantly alter litter size, pup body weight, or anogenital distance compared to vehicle-treated controls. Histological analysis revealed abnormal testis morphology in 50% of testes exposed to 50 µg/kg/day of BPA and 80% of testes in the 0.05 µg/kg/day DES and 0.5 µg/kg/day BPA treatment groups. Dysgenic BPA- and DES-exposed testes contained fewer testis cord cross-sections and increased interstitial area compared to vehicle controls. Underdevelopment of the testis cords was particularly evident near the rete testes, where uncoiled lengths of testis cord appeared as finger-like projections. Thus, our study indicates in utero exposure to BPA doses equal to or below the FDA acceptable daily intake value of 50 µg/kg/day can alter fetal testis development in the mouse. Furthermore, the histological similarities between DES- and BPA-exposed testes suggested BPA-induced changes in testis cord development are likely mediated by ERalpha. Surprisingly, altered testis histology following low-dose BPA or DES treatment was remarkably similar in appearance to the fetal testis cord dysgenesis we observed in conditional knockout (cKO) mice lacking expression of inhibin betaA (Inhba), a subunit of activin A, in the fetal Leydig cells. Loss of fetal Leydig cell-derived activin A leads to decreased Sertoli cell proliferation and subsequent impairment of testis cord expansion. Murine fetal Leydig cells express ERalpha, suggesting exposure to estrogenic compounds could potentially influence fetal Leydig cell expression of Inhba/activin A. We therefore hypothesized that BPA- and DES-induced testis cord dysgenesis results from alteration of fetal Leydig cell expression of Inhba and/or disruption of activin A signaling. We are currently testing our hypothesis by performing quantitative real-time PCR analysis for genes involved in the testicular activin A signaling pathway. This research was supported by NIH 1P20ES018163 and NIH T32ES07326. (poster)

Bisphenol-A (BPA) is a synthetic xenoestrogen used in polycarbonate plastics, food and beverage can liners, epoxy resins, toys, and dental sealants. BPA is present in 95% of tested human urine samples. As a potent estrogenic endocrine disruptor, BPA may adversely affect female reproductive system development, especially in low, environmentally relevant doses. However, few studies have examined the effects of low-dose BPA exposure on female reproductive system development, particularly ovaries. Previous studies have shown that oocytes from low-dose in utero-BPA exposed female fetuses display gross aberrations in meiotic prophase, including synaptic defects and increased levels of recombination. Oocytes are integral parts of primordial follicles. Mammalian females are born with a finite number of primordial follicles, of which a small fraction survives, while most die via apoptosis. Further depletion of primordial follicles could have deleterious effects on fertility and lead to a wide range of hormone-related diseases such as osteoporosis, early menopause, and cardiovascular disease. This study tested the hypothesis that in utero low dose BPA exposure (0.5 μg/kg and 50 μg/kg) changes the ovarian morphology and reduces the number of primordial follicles at birth. To test this hypothesis, CD-1 dams were dosed orally with BPA (0.5 μg/kg and 50 μg/kg) or tocopherol-stripped corn oil as a vehicle during the critical period of gonad development (embryonic day 10.5 to day 17.5). Ovaries were isolated from pups delivered by Caesarian section by embryonic day 19.0. Ovaries were then processed for histological evaluation using hematoxylin and eosin stains. Primordial follicles were counted in every 10th section. The results indicate that the ovaries from BPA exposed mice were less cellular with more dense and congested vasculization than ovaries from vehicle exposed mice. The percentage of healthy primordial follicles in the BPA exposed ovaries was significantly reduced compared to the vehicle control (vehicle control = 83.81 ± 1.99%; BPA 0.5 μg/kg/day = 64 ± 3.36%; BPA 50 μg/kg/day = 72.45 ± 1.65%, n=3, p<0.05). Further, the percentage of abnormal primordial follicles in the BPA exposed ovaries was significantly increased compared to the vehicle control (vehicle control = 16.19 ± 1.99%; BPA 0.5 μg/kg/day = 36 ± 3.36%; BPA 50 μg/kg/day = 27.55 ± 1.65%, n=3, p<0.05). Collectively, these data indicate that exposure to low levels of BPA in utero could affect the development of the ovary. This ovarian developmental defect could further affect the reproductive life of females born to BPA exposed mothers. Support: NIH T32ES07326 and NIH 1P20ES018163. (platform)

At birth, the ovaries contain a finite number of primordial follicles. Only a limited number of these primordial follicles will mature into antral follicles. Antral follicles are essential for the proper functioning of the ovary because they synthesize and secrete sex steroid hormones important for the maintenance and regulation of estrous cyclicity and fertility. Di-(2-ethylhexyl) phthalate (DEHP) is a plasticizer found in many commercially used products such as plastic bottles, IV tubes, toys, fragrances and cosmetics. DEHP, a toxic parent compound, can be metabolized by esterases in the body to form mono-(2-ethylhexyl) phthalate (MEHP). MEHP is known to restrict growth, reduce estradiol levels and cause death of antral follicles via apoptosis. Many pathways can lead to cell death via apoptosis, but oxidative stress is a pathway specifically known to cause apoptosis in both non-reproductive and reproductive tissues. Balance between reactive oxygen species production and detoxification by antioxidant enzymes such as Cu/Zn superoxide dismutase (SOD1), glutathione peroxidase (GPX), and catalase (CAT) keep the cell in a healthy and reduced state. Any environmental toxicant exposure that disrupts this balance results in oxidative stress in the cell. Since it was not known if MEHP induces oxidative stress in antral follicles, the goal of this study was to test the hypothesis that MEHP induces the oxidative stress pathway by suppressing the expression of SOD1, GPX and CAT in antral follicles. To test this hypothesis, antral follicles were mechanically isolated from adult cycling CD-1 mice and cultured for 96 hours in alpha-minimal essential media containing either MEHP (0.1-10 µg/ml) or the vehicle control, dimethylsulfoxide (DMSO). Following culture, follicles were subjected to quantitative real time PCR to measure mRNA levels of the Sod1, Gpx, and Cat genes. The results indicate that MEHP significantly decreased mRNA expression of Sod1 compared to controls (DMSO=67.33±8.51 genomic equivalents (GE), MEHP 0.1 µg/ml=24.03±7.73 GE, MEHP 1 µg/ml=19.03 ±4.25 GE, MEHP 10µg/ml=18.73 ±9.41 GE; n=3; p≤0.05). In addition, MEHP significantly decreased mRNA levels of the Gpx gene compared to controls (DMSO=29.16±3.99 GE, MEHP 0.1 µg/ml=3.69±0.45 GE, MEHP 1 µg/ml=4.90±2.04 GE, MEHP 10 µg/ml=2.47±0.60 GE; n=3; p≤0.05). However, the expression levels of Cat were not significantly affected by MEHP exposure compared to controls (DMSO=9.78±0.81 GE, MEHP 0.1 µg/ml=3.85±2.13 GE, MEHP 1 µg/ml=3.47±1.21 GE, MEHP 10µg/ml=4.47±1.77 GE; n=3). Therefore, it is possible that MEHP represses the expression of specific antioxidant enzymes, allowing apoptosis of antral follicles via the oxidative stress pathway. Support: R01ES012893; T32ES07326. (poster)

The aryl hydrocarbon receptor (AHR) is a ligand-activated transcription factor that mediates the toxicity of environmental chemicals and regulates many physiological functions, including processes in female reproduction. Previous studies demonstrated that Ahr deletion leads to slow ovarian follicle growth because of impaired estradiol production and reduced gonadotropin responsiveness in prepubertal mice. These studies, however, did not determine how Ahr deletion impairs estradiol production or whether the effects of Ahr deletion on follicle growth and estradiol production persist in adulthood. Thus, the present study evaluated the effect of Ahr deletion on steroid precursors in the estradiol biosynthesis pathway. Furthermore, this study evaluated follicle growth and estradiol biosynthesis in wild-type (WT) and Ahr knockout (AhrKO) antral follicles at different stages of sexual maturity. AhrKO antral follicles from prepubertal mice had slower growth, produced lower estradiol levels, and had reduced cyclin D2 (Ccnd2) expression compared to WT follicles. AhrKO follicles from adult mice, however, produced higher androgen levels and expressed higher levels of Ccnd2 compared to WT follicles. Furthermore, AhrKO follicles from adult mice had growth to that of WT follicles. These findings suggest that the AHR regulates follicle growth by altering factors involved in the estradiol biosynthesis pathway as well as key regulators of follicle growth and that this role of AHR depends on stage of sexual maturity.