Effects of Low Doses of Pesticides on the Hemomicrocirculatory Bed and Tissue Structures of the Uterus in Rats During Early Postnatal Ontogenesis

Abstract

Background. Synthetic pyrethroids remain among the most widely applied insecticides in intensive agriculture. Vantex, a gamma-cyhalothrin formulation, combines high insecticidal potency with the capacity for transplacental and lactational transfer, which places the developing female reproductive tract at particular risk. The microvascular component of this injury has rarely been reconstructed morphologically.
Objective. To characterise postnatal morphogenesis of the hemomicrocirculatory bed and the tissue structures of the uterus and ovary in offspring born to dams with chronic low-dose Vantex intoxication, and to assess proliferative (Ki-67) and anti-apoptotic (Bcl-2) immunoreactivity.
Materials and methods. Outbred white rats were allocated to two groups of 30 dams each: intact controls and dams receiving Vantex at 4.0 mg/kg body weight per day by oral administration throughout gestation and lactation. Offspring were examined on postnatal days (PND) 7, 14, 21 and 30. Uterine angioarchitecture was visualised after infusion of Gerota mass through the abdominal aorta followed by clearing according to Sagatov. Paraffin sections 5–7 µm thick were stained with haematoxylin and eosin. Ki-67 and Bcl-2 were demonstrated with monoclonal antibodies on a Ventana BenchMark XT platform using 3,3ʹ-diaminobenzidine chromogen. Evaluation was qualitative and semi-quantitative; no inferential statistical testing was performed.
Results. Maternal Vantex exposure produced inflammatory-destructive remodelling of utero-ovarian microvessels, condensation of stromal collagen and elastic fibres, premature atresia of centrally placed oocytes, thecal dystrophy, necrotic foci among luteocytes, and blunting of the physiological expansion of the uterine venous bed. Medullary venule lumen was approximately 1.3-fold wider than in controls by PND 21. Ki-67 labelling increased in isthmicocervical glandular epithelium and in ovarian parenchyma and stroma; Bcl-2 remained clearly positive at PND 30. Vascular change was detectable before overt parenchymal destruction.
Conclusions. In this mother–offspring model, Vantex behaves as a reproductive toxicant whose tissue injury is tightly coupled to failure of the hemomicrocirculatory bed. Juvenile morphological endpoints that include angioarchitecture deserve consideration in the assessment of modern pyrethroids, and preventive measures are warranted for populations with chronic pyrethroid exposure.