The role of stimulator of interferon genes‐mediated AMPK/mTOR/P70S6K autophagy pathway in cyfluthrin‐induced testicular injury

Abstract

Cyfluthrin is widely used in the field of sanitary pest control by its wide insecticidal spectrum, high efficiency and low toxicity, low residue, and good biodegradability. But, as a double‐edged sword, a large amount of cyfluthrin remains are still in the environment. The residual cyfluthrin is absorbed into the food chain through vegetation and then poses a risk to soil organisms and human health. Several studies have suggested that cyfluthrin is one of the main factors causing testicular damage, but the mechanism remains unclear. In this study, we established in vivo and in vitro models of testicular injury in rats and GC‐2 cells exposed to cyfluthrin to explore whether stimulator of interferon genes (STING) gene mediates the regulation of AMPK/mTOR/p70S6K autophagy pathway, which lays a foundation for further study of the mechanism of testicular injury induced by cyfluthrin. The results showed that the activity of super oxide dismutase in testis decreased and the activity of malonic dialdehyde increased with the increase of concentration in vivo and in vitro. At the same time, the levels of mitochondrial damage and inflammation in the testis also increased, which further activated autophagy. In this process, the increased level of inflammation is related to the increased expression of STING gene, and AMPK/mTOR/p70S6K autophagy pathway is also involved. To sum up, cyfluthrin has certain reproductive toxicity, and long‐term exposure can induce testicular cell damage. STING gene can participate in cyfluthrin‐induced testicular injury through AMPK/mTOR/P70S6K autophagy pathway.

The Role of G3BP1 Gene Mediates P38 MAPK/JNK Pathway in Testicular Spermatogenic Dysfunction Caused by Cyfluthrin

“…At present, at least three MAPK families have been identified: extracellular signal-regulated kinase 1/2 (ERK 1/2), c-Jun N-terminal kinase (JNK) and p38 mitogen-activated protein kinase (P38 MAPK) [ 24 ]. Our previous study showed that the expression of INHα and INHβB proteins in the testes of rats was reduced after being poisoned with Cy, suggesting that the testes may be the target organ of Cy toxicity, as, to some extent, it interferes with the normal secretion and function of male hormones, changes the hormone level and causes the stable state of the male reproductive endocrine system to break [ 25 ]. Therefore, the testicular spermatogenic function can be determined by the detection of reproductive hormones, and the normal signal transduction of the hypothalamus–pituitary–gonad axis is also strongly associated with the MAPK pathway.…”

Effects of Cyfluthrin Exposure on Neurobehaviour, Hippocampal Tissue and Synaptic Plasticity in Wistar Rats

“…With the increasing use of Cy, the potential health effects of Cy residues on soil organisms and human beings have become a hot issue [ 3 ]. The accumulation of Cy in the body causes disorders of the nervous system, digestive system, reproductive system, cardiovascular system and immune system [ 4 , 5 , 6 , 7 ]. Moreover, a previous research group found that approximately 57% of the investigated vegetable greenhouse growers used dangerous concentrations of Cy, which were higher than those of other pyrethroid insecticides used [ 8 ].…”