Environmental and occupational exposure to cadmium has been shown to induce kidney damage, liver injury, neurodegenerative disease, and osteoporosis. However, the mechanism by which cadmium induces autophagy in these diseases remains unclear. Studies have shown that cadmium is an effective inducer of oxidative stress, DNA damage, ER stress, and autophagy, which are thought to be adaptive stress responses that allow cells exposed to cadmium to survive in an adverse environment. However, excessive stress will cause tissue damage by inducing apoptosis, pyroptosis, and ferroptosis. Evidently, oxidative stress-induced autophagy plays different roles in low- or high-dose cadmium exposure-induced cell damage, either causing apoptosis, pyroptosis, and ferroptosis or inducing cell survival. Meanwhile, different cell types have different sensitivities to cadmium, which ultimately determines the fate of the cell. In this review, we provided a detailed survey of the current literature on autophagy in cadmium-induced tissue damage. A better understanding of the complex regulation of cell death by autophagy might contribute to the development of novel preventive and therapeutic strategies to treat acute and chronic cadmium toxicity.

Cadmium is a heavy toxic metal with unknown biological functions in the human body. Over time, cadmium accretion in the different visceral organs (liver, lungs, kidney, and testis) is said to impair the function of these organs, which is associated with a relatively long biological half-life and a very low rate of excretion. Recently studies have revealed that the testes are highly sensitive to cadmium. In this review, we discussed the adverse effect of cadmium on the development and biological functions of the testis. The Sertoli cells (SCs), seminiferous tubules, and Blood Testis Barrier are severely structurally damaged by cadmium, which results in sperm loss. The development and function of Leydig cells are hindered by cadmium, which also induces Leydig cell tumors. The testis’s vascular system is severely disturbed by cadmium. Cadmium also perturbs the function of somatic cells and germ cells through epigenetic regulation, giving rise to infertile or sub-fertile males. In addition, we also summarized the other findings related to cadmium-induced oxidative toxicity, apoptotic toxicity, and autophagic toxicity, along with their possible mechanisms in the testicular tissue of different animal species. Consequently, cadmium represents a high-risk factor for male fertility.

Cadmium (Cd) is a pervasive environmental and industrial toxin that poses significant health risks. It readily moves through soil–plant systems, leading to global contamination and human exposure through diet, smoking, and pollution. The main purpose of this review is to explore the effect of Cd on physiological processes of different bodies’ organs, including the bones, kidneys, and liver, as well as the immune, cerebrovascular, cardiovascular, and reproductive systems. Accumulation of Cd in the body can result in poisoning with severe impacts on bone and kidney health, as well as reduced bone mineral density due to renal damage. Research has linked Cd to lung cancer and pulmonary toxicity, and elevated urinary biomarkers suggest compromised renal function. Cd also affects the cardiovascular, cerebrovascular, and immune systems; the liver; and reproductive systems, contributing to various diseases by disrupting blood pressure and calcium regulation, causing oxidative stress and DNA damage, and impairing cell functions. Ongoing research is essential to fully understand Cd-induced toxicological effects and to develop effective interventions to prevent exposure and mitigate health risks.

Microplastics have become a new type of environmental pollutant that can accumulate in various tissues and organs of the body and cause chronic damage. In this study, two different size polystyrene microplastics (PS-MPs, 5 μm and 0.5 μm) exposure models were established in mice to investigate the effects of PS-MPs with different particle sizes on oxidative stress in the liver. The results showed that PS-MPs exposure caused a decrease in body weight and liver-to-body weight. The hematoxylin and eosin staining and transmission electron microscopy results showed that exposure to PS-MPs led to the disorganized cellular structure of liver tissue, nuclear crinkling, and mitochondrial vacuolation. The extent of damage in the 5 μm PS-MP exposure group was more extensive when compared with the other group. The evaluation of oxidative-stress-related indicators showed that PS-MPs exposure exacerbated oxidative stress in hepatocytes, especially in the 5 μm PS-MPs group. The expression of oxidative-stress-related proteins sirtuin 3(SIRT3) and superoxide dismutase (SOD2) was significantly reduced, and the reduction was more pronounced in the 5 μm PS-MPs group. In conclusion, PS-MPs exposure led to oxidative stress in mouse hepatocytes and caused more severe damage in the 5 μm PS-MPs group when compared with the 0.5 μm PS-MPs group.

Cadmium (Cd) is a potential pathogenic factor in the urinary system that is associated with various kidney diseases. Microplastics (MPs), comprising of plastic particles less than 5 mm in diameter, are a major carrier of contaminants. We applied 10 mg/L particle 5 μm MPs and 50 mg/L CdCl2 in water for three months in vivo assay to assess the damaging effects of MPs and Cd exposure on the kidney. In vivo tests showed that MPs exacerbated Cd-induced kidney injury. In addition, the involvement of oxidative stress, autophagy, apoptosis, and fibrosis in the damaging effects of MPs and Cd on mouse kidneys were investigated. The results showed that MPs aggravated Cd-induced kidney injury by enhancing oxidative stress, autophagy, apoptosis, and fibrosis. These findings provide new insights into the toxic effects of MPs on the mouse kidney.