Advantix, Advantage, Seresto: Inhibits Male Reproduction and Harms Mitochondria (cellular health)
(please be reminded, there is also new evidence that suggests human children and people are also absorbing these chemicals into the blood stream and chemicals are making their way to water supplies) Go Natural. Detox often.
https://www.sciencedirect.com/science/article/pii/S1382668923002521
"Imidacloprid is a systemic neonicotinoid insecticide widely used to combat agricultural pests and even flea infestation in dogs and cats (Ensley, 2018, Tomizawa and Casida, 2005). The neonicotinoids have a greater affinity for nicotinic acetylcholine receptors (nAChRs) of insects than vertebrates (Tomizawa and Casida, 2005), therefore, it is thought to be less toxic for mammals (Millot et al., 2017). Imidacloprid is registered worldwide as a pesticide to protect various crops (Shao et al., 2013). In 2020, pharmaceutical companies produced approximately 20,000 tons (Simon-Delso et al., 2015). However, the extensive use of imidacloprid resulted in toxicity in non-target organisms such as bees (Cresswell, 2011), and birds (Hallmann et al., 2014), consequently, its use as seed treatment was prohibited by the European Union in 2013 (European Commission, 2013). The consumption of imidacloprid-treated seed in France has been linked to several mortality events among birds between 1995 and 2014 (Millot et al., 2017). A similar adverse effect of imidacloprid on wild granivorous birds was observed in South Africa’s Western Cape province by Botha et al. (2018).
Furthermore, it has been reported that imidacloprid induces male reproductive toxicity (Bal et al., 2012a, Bal et al., 2012b, Hafez et al., 2016, Lonare et al., 2016, Najafi et al., 2010), leading to infertility. Imidacloprid causes a decrease in the number, motility, and viability of sperm in adult Wistar rats (Lonare et al., 2016, Najafi et al., 2010), and albino rats (Hafez et al., 2016). The adverse effects of imidacloprid were attributed to oxidative stress and an increase in polyunsaturated fatty acids caused the decline in Leydig cells, which resulted in a decrease in testosterone levels (Bal et al., 2012a, Bal et al., 2012b).
Discussion
In recent years, global concerns grew regarding the decline of male reproductive capability (Tong et al., 2022). Studies have confirmed that exposure to environmental toxicants might be one of the primary reasons (Mann et al., 2020, Mendy and Pinney, 2022). Imidacloprid, a neonicotinoid insecticide, is highly soluble in water, therefore it can easily accumulate in ground and surface water causing adverse environmental effects (Demirak, 2019, Hrybova et al., 2019, Tišler et al., 2009). It has been reported that exposure to imidacloprid affects male fertility in rabbits and rats (Alamgir Kobir et al., 2023, Saber et al., 2021). Leydig cells are responsible for testosterone synthesis to maintain spermatogenesis and reproductive fitness and are susceptible to environmental toxicants (Chen et al., 2010, Zhang et al., 2022b), including imidacloprid (Bal et al., 2012b, Zhao et al., 2021). In the current study, imidacloprid had a cytotoxic effect on Leydig cells in vitro (Fig. 1). To our knowledge, there have been no studies reporting the cytotoxic effects of imidacloprid on the Leydig cell line; but it has been reported that imidacloprid caused cytotoxicity in a human hepatoblastoma (HepG2) cell line (Conte et al., 2022, Guimarães et al., 2022), human prostate epithelial (WPM-Y.1) cell line (Abdel-Halim and Osman, 2020), and Chinese hamster ovary (CHO-K1) cell line (Al-Sarar et al., 2015). Among these, Conte et al. (2022) reported that exposure to a commercial formulation of imidacloprid (60% purity) at 663.66 mg/L (2654.64 µM) induced a 50% effect in HepG2 cells after 48 h. Other authors also indicated that exposure to the pure form of 500–2000 µM imidacloprid for 24 and 48 h induced a significant decrease in HepG2 cell viability (Guimarães et al., 2022). In the present study, a notable reduction in the viability of cells treated with imidacloprid concentrations of 800 µM for 48 h or above 300 µM for 72 h, based on the MTT assay, was observed, and was also confirmed with the alamarBlue® assay. The MTT assay evaluates the mitochondrial activity, while the alamarBlue® assay measures the total cell viability, thus verifying that Leydig cells are indeed susceptible to toxicity induced by imidacloprid."
