Abstract
Cadmium is a nonessential metal that has heavily polluted the environment due to human activities. It can be absorbed into the human body via the gastrointestinal tract, respiratory tract, and the skin, and can cause chronic damage to the kidneys. The main site where cadmium accumulates and causes damage within the nephrons is the proximal tubule. This accumulation can induce dysfunction of the mitochondrial electron transport chain, leading to electron leakage and production of reactive oxygen species (ROS). Cadmium may also impair the function of NADPH oxidase, resulting in another source of ROS. These ROS together can cause oxidative damage to DNA, proteins, and lipids, triggering epithelial cell death and a decline in kidney function. In this article, we also reviewed evidence that the antioxidant power of plant extracts, herbal medicines, and pharmacological agents could ameliorate cadmium-induced kidney injury. Finally, a model of cadmium-induced kidney injury, centering on the notion that oxidative damage is a unifying mechanism of cadmium renal toxicity, is also presented. Given that cadmium exposure is inevitable, further studies using animal models are warranted for a detailed understanding of the mechanism underlying cadmium induced ROS production, and for the identification of more therapeutic targets.
Highlights
The kidney is a vital organ that performs critical physiological functions by actively filtering excess fluid and secreting waste products including urea, uric acid, and creatinine [1,2]
We reviewed evidence that the antioxidant power of plant extracts, herbal medicines, and pharmacological agents could ameliorate cadmium-induced kidney injury
Mechanisms of Cadmium-Induced Renal Toxicity What is the proposed mechanism of cadmium-induced kidney injury? Based on numerous studies, all injurious pathways converge on reactive oxygen species (ROS) production and culminate in oxidative stress [77,78,79,80,81], which suggests that oxidative damage is a unifying mechanism of cadmiuminduced renal toxicity and injury
Summary
The kidney is a vital organ that performs critical physiological functions by actively filtering excess fluid and secreting waste products including urea, uric acid, and creatinine [1,2]. Cadmium exposure has been tightly associated with renal dysfunction and kidney damage, causing polyuria and proteinuria [23,24]. The proximal tubule is the major site of cadmium deposition, accumulation, and damage because of the epithelial cell hypertrophy with occurrence of polyuria and proteinuria [44,45,46]. Development of proximal tubular epithelial cell hypertrophy with occurrence of polyuria itand is important counteract cadmium-induced injury to safeguard kidney proteinuria to [44,45,46]. Cadmium has a highTransportation, affinity towardand thiolAccumulation groups and can
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