Malathion Affects Spermatogenic Proliferation in Mouse

Abstract

SUMMARY:The restriction of the mechanisms of cell proliferation in murine seminiferous epithelium, in terms of induction of programmed cell death until recently has not been fully analyzed. The aim of this work was to assess the effect of Malathion (MP) on testicular morphology and function in mouse spermatogenesis. For the experiments, male albino mice of strain NMRI-IVIC, weighing between 30-40 g were used, and divided into control and experimental groups of 5 each. The animals of the experimental groups were injected with a single dose of MP: 241mg/kg weight (1/12 LD 50 ) resuspended in 0.9% saline, intraperitoneally. Animals were sacrificed at 8.3, 16.6 and 33.2 days post-injection (first, second and third spermatogenic cycles). Testicular samples were obtained for light microscopy (LM), transmission electron microscopy procedures, and to detect apoptosis and p53 antigen by immunohistochemical methods. Blood was collected to quantify testosterone and plasmatic cholinesterase activity. From 8.3 days, Sertoli cell vacuolization, karyolisis of pachytene spermatocytes and Leydig cells and a decreased in average of the diameter of seminiferous tubules was observed. No damage to inter-Sertoli cells junctions was detected. Percentage of seminiferous tubules showing germ cells apoptosis was increased from 8.3 days, plasmatic acetylcholinesterase activity was reduced in the group treated only 24 hours after administration of MP. Serum testosterone levels were low in treated animals at 16. 6 and 33.2 days. p53 was mostly expressed in pachytene spermatocytes from 8d. The findings of this study indicate that MP alters the testicular function affecting the DNA and interfering with spermatogenesis as well as steroidogenesis.

Organophosphate toxicity: updates of malathion potential toxic effects in mammals and potential treatments

“…ROS may induce DNA damage and activates apoptotic pathways. It has been found that MAL disrupts the seminiferous epithelium proliferation, by impairing steroidogenesis, and that induces DNA fragmentation and apoptosis (Penna-Videau et al 2012;Bhardwaj et al 2018). MAL-induced increase in spermatogenic apoptosis rate was confirmed by modified protein expression of p53, Bax, and Bcl-2, which facilitate apoptosis initiation (Penna-Videau et al 2012;Bhardwaj et al 2018).…”

“…It has been found that MAL disrupts the seminiferous epithelium proliferation, by impairing steroidogenesis, and that induces DNA fragmentation and apoptosis (Penna-Videau et al 2012;Bhardwaj et al 2018). MAL-induced increase in spermatogenic apoptosis rate was confirmed by modified protein expression of p53, Bax, and Bcl-2, which facilitate apoptosis initiation (Penna-Videau et al 2012;Bhardwaj et al 2018). Although it has been documented that MAL exerts its cytotoxic outcomes, via direct effects on mitochondria by the induction of apoptosis, which may be due to increased ROS activating apoptotic pathways, the apoptotic effects may also be explained in terms of MAL-genotoxic effects that alter gene expression without mutation (Geng et al 2015a(Geng et al , 2016.…”

“…Although it has been documented that MAL exerts its cytotoxic outcomes, via direct effects on mitochondria by the induction of apoptosis, which may be due to increased ROS activating apoptotic pathways, the apoptotic effects may also be explained in terms of MAL-genotoxic effects that alter gene expression without mutation (Geng et al 2015a(Geng et al , 2016. Another possible mechanism may be the induction of RNA and DNA alkylation, leading to mutagenesis, sperm morphology disruption, or teratozoospermia (associated with a high risk of apoptosis) (Agarwal and Said 2005;Penna-Videau et al 2012). Thus, the decreased number of sperm cells and spermatozoon may be caused by increased apoptosis associated with MAL exposure (Geng et al 2015a(Geng et al , 2015b.…”

Malathion induced testicular toxicity and oxidative damage in male mice: the protective effect of curcumin

“…Leydig and spermatogenic cell degeneration might occur in this condition as a result of the oxidative damage, which decreases the sperm counts and deactivates spermatogenesis (Uzunhisarcikli et al 2007;Penna-Videau et al 2012). Penna-Videau and his colleagues reported that steroidogenesis is impaired by malathion exposure and this in turn stimulates the proliferation of the seminiferous epithelium beside the apoptosis that affect germ cells (Penna-Videau et al 2012). Moreover, reduced chromatin and damaged DNA can be caused by malathion exposure that affect the maturation of spermatogenic cells in mice in its late stages (Ojha and Srivastava 2014;Moore et al 2011).…”

Bisphenol A-induced ultrastructural changes in the testes of common marmoset

“…These included condensation of chromatin material, presence of more than two nuclei, disappearance of the nuclear envelope and numerous apoptotic changes. Similar effects were induced by other compounds such as malathion 20 and cadmium 21 . BPA caused degenerative changes in the form of vacuolation, membrane thickening and deformed basement membrane.…”