Browsing by Subject "Thyroid hormones"

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    Effects of photo stimulation and nonstimulation of golden hamsters (Mesocricetus auratus) from birth to early puberty on testes structure and function
    (Murcia : F. Hernández, 2009) Hance, Michael W.; Mason, J.Ian; Chamindrani Mendis-Handagama, S.M.L.
    We tested whether puberty in golden hamsters is photoperiodically controlled. Hamsters were raised under 14:10 hours Light:Dark (14L) and 1:23 hours Light:Dark (1L) respectively, from birth to 28 days and tested for various parameters. Body weight, Leydig cell (LC) size and testicular testosterone secretion were greater and plasma thyroxin (T4), testicular androstenedione secretion and LC number were lower (P<0.05) in 1L than 14L hamsters. Volumes of testicular components were similar in the two groups. 3ß-hydroxy steroid dehydrogenase immunohistochemistry demonstrated LC progenitors and newly formed adult LC (ALC) in 14L hamsters, which were absent in 1L hamsters; they contained only fetal LC (FLC). Latter findings suggest the presence and absence of postnatally-differerentiated LC in 14L and 1L hamsters, respectively. Androgen results agreed with these findings, because FLC primarily secrete testosterone, and androstenedione is a major androgen secreted by the newly formed ALC. Reduced T4 in 1L hamsters is attributed to the inhibition of thyroid function by the increased duration of melatonin secretion due to non-photostimulatory conditions. The arrest in LC differentiation in 1L hamsters is attributed to low T4 levels. Although the testis size is unaltered under nonphotostimulatory conditions, postnatal LC differentiation is inhibited in golden hamsters, and therefore, it is logical to suggest that their puberty is photoperiodically controlled.
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    Maternal exposure to the environmental pollutant "BDE-47" impairs the postnatal development of rat cerebellar cortex by modulating neuronal proliferation, synaptogenesis, NGF and BDNF pathways
    (Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2022) Mandour, Dalia A.; Tolba, Asmaa M; El Bestawy, Emtethal M.
    . 2,2’,4,4’-Tetrabromodiphenyl ether (BDE47) is an environmental contaminant that crosses the blood placental barrier and interferes with the homeostasis of fetal thyroid hormones. Aim of work. This study was designed to investigate the perinatal effect of BDE-47 exposure on the postnatal development of the rat cerebellar cortex. Materials and methods. This study was carried out on 20 pregnant rats and 36 of their offspring. The pregnant rats were divided equally into control and BDE-47 treated mother groups; supplemented orally with BDE-47 (0.2 mg/kg/day from day 8 of gestation until the day of weaning). The offspring of both mother groups were subdivided, according to their developmental age, into three subgroups; PND14, PND21and PND42. SerumT3, T4 and TSH were assessed for dams and their offspring. Testing the motor coordination of the offspring via the rotarod test was conducted. Sections of the cerebellar cortex from offspring subgroups were stained with hematoxylin and eosin alongside immunohistochemical reactions and optical density of nerve growth factor (NGF), brain derived neurotrophic factor (BDNF), proliferating cell nuclear antigen (PCNA) and synaptophysin (SYN) were assessed. Also, the thickness of different layers of the cerebellar cortex was histomorphometrically measured. Results. BDE-47 treated mothers and their offspring subgroups showed a significant decrease in the serum free T3, T4 and increased TSH. The BDE-47 offspring displayed incoordination of the motor activity together with disturbed cytoarchitecture of the cerebellar cortical layers, and impaired migration of its germinative neuronal zones, particularly on PND14 and PND21. Moreover, these offspring displayed a decrease of the immune-expression and optical density of NGF, BDNF in the cerebellar cortical layers with impaired proliferation, and synaptogenesis. Conclusion. Maternal exposure to BDE-47 during pregnancy and lactation effectuated a potential deleterious retarding effect on the postnatal development of the rat cerebellar cortex mostly via modulating neuronal proliferation, synaptogenesis, NGF and BDNF pathways secondary to its hypothyroid effect.