The Effect Of Cadmium Stress And Bacterial Infection On Mitochondrial Function In Musca Domestica

Mitochondria are involved in many important physiological processes,including intracellular three carboxylic acid cycle,fatty acid metabolism and oxidative phosphorylation.Mitochondrial dysfunction is closely related to many metabolic diseases such as diabetes,tumor and neuropathic disease.Environmental stress stimulation and biological stress challenge are two common methods to induce oxidative stress in organisms.In this work,cadmium and bacteria stimulation were selected to study the mechanism of mitochondrial damage in housefly.Moreover,mitochondrial respiratory chain activity and oxidative phosphorylation efficiency were also investigated extensivly.Firstly,we studied on an important biomarkers 8-hydroxyguanine DNA glycosidase gene(8-Oxoguanine DNA Glycosylase,OGG1)in M.domestica.OGG1 is closely related to the repair of mitochondrial DNA damage.We use real-time fluorescence quantitative PCR and Western Blot methods to analysis the changes of OGG1 at different developmental stages and tissues in M.domestica.Then the expression of OGG1 was examined under different stimulation(ultraviolet,Adriamycin,cadmium chloride and bacteria).The results showed that the content of 8-oxoG in M.domestica eggs and fat bodies was relatively high.In addition,the upregulated expression of OGG1 was observed after UV exposure,which indicated that OGG1 is involved in the oxidative stress repair process in M.domestica.Secondly,we stimulated the effect of heavy metal cadmium on M.domestica.A mitochondrial damage model was establish,the mechanism of polyphenols antioxidant polydatin on mitochondrial damage respairment was investigated.The results showed that cadmium chloride could induce the oxidative stress response in M.domestica.MDA content in M.domestica was increased and the activity of SOD was decreased significantly.Moreover,the mitochondria in M.domestica were obviously damaged by cadmium chloride: 8-oxoG(mitochondrial DNA damage marker)content increased,mitochondrial membrane potentialdecreased and the mitochondrial respiratory chain complex decreased.Intrestingly,polydatin can significantly restore mitochondrial damage induced by cadmium chloride in M.domestica.Finally,two bacteria(Escherichia coli and Staphylococcus aureus)were selected to stimulate housefly larvae.The relationship between immune stress stimulation and mitochondrial damage was explored.We found that the content of MDA and ROS in larvae were increased after bacterial stimulation.The results indicated that bacterial stimulation induced oxidative damage in larvae.After bacterial stimulation to housefly larvae,the decrease of mitochondrial membrane potential and mtDNA copy number were observed,while the increase of 8-oxoG was detected.The results confirmed the existence of mitochondria damaged in larvae.At the same time,bacterial stimulation also caused the changes of mitochondrial respiratory chain complex activity and oxidative phosphorylation efficiency in housefly larvae.The activity of complex I and complex II were decreased,the respiratory control rate(RCR)and phosphorus oxygen ratio(ADP/O)were increased.This inferred that bacterial stimuli could cause mitochondrial damage and respiratory chain efficiency.Housefly larvae was deduced to synthesize sufficient ATP to increase the oxidative phosphorylation efficiency for compensating bacterial infection.This study illuminated the relationship between bacterial stimulation and mitochondrial damage in M.domestica.