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Problem statement: Cadmium is highly toxic at low concentrations, but the mechanism of its toxicity is still not understood particularly at the cellular and subcellular level. Approach: In this study we examined the effects of cadmium on the oxidophosphorylation properties of mitochondria isolated from potatoes. Results: Cadmium strongly disturbed the respiratory metabolism of mitochondria isolated especially in the transfer of electrons by cyanide pathway. Meanwhile, cadmium altered the composition of lipid fatty acids polar while inhibiting catalase activity, a key enzyme in the detoxification (antioxidant) process. In addition, cadmium caused an increase in mitochondrial volume associated with strong inhibition of ATPase activity, which could be explained by a transport of the potassium ion stimulation at the origin of the massive influx of H + by antiport through the K + /H + leading to a decoupling (cut) of mitochondrial oxidative phosphorylation. The swelling of mitochondria was accompanied by the rupture of the mitochondrial outer membrane and thus the release of Cytochrome C, which appears to be the initial phase of apoptosis. Conclusion: Following this study, it appeared that cadmium generates in potato the isolated mitochondria a concentrationdependent oxidative stress.

In this study, adult snails, Helix aspersa were used to estimate the effect of aneonicotinoid insecticide (thiametoxam) on biochemical parameters and histological changes in the hepatopancreas of this gastropod after a treatment of six weeks. During this period, snails were exposed by ingestion and contact to fresh lettuce leaves which were soaked with an insecticide solution. The thiametoxam test solutions were 0, 25, 50, 100 and 200 mg/L. The results of the biochemical dosages (total carbohydrates, total proteins and total lipids) showed significant decreases at two concentrations (100 and 200 mg/L) of thiametoxam. However, the histological examination of the hepatopancreas of the treated snails showed alterations as a response to all the treatments, and revealed the degeneration of the digestive tubules and the breakdown of the basement membrane in a dose-dependent manner, leading to a severe deterioration of the tissues in the concentration of 200 mg/L thiametoxam. The dosage of carbohydrates, lipids and proteins supported by the study of histological changes on the hepatopancreas of H. aspersa can be considered as potential biomarkers of exposure to thiametoxam.

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