Cd is a non-degradable heavy metal pollutant with no known biological role. When taken up by living organisms from the environment, it causes extensive tissue damage. Here, we studied the effects of exposure to 20 mg/L⁻¹CdCl₂for 0, 24, 48, and 72 h on the renal tissue of marine catfish Arius arius. Cd uptake, metallothionein (MT) induction, microarchitectural alterations, DNA fragmentation, and caspase-3 activity were studied. Cd and MT levels were time-dependent and positively correlated. The diameter of the Bowman's capsule and tubules was significantly increased. Meanwhile, the density, diameter, and volume of the glomerulus as well as the density and volume of tubules decreased. Cd induced apoptosis though elevatedcaspase-3 activity. These results support the notion that exposure to sublethal Cd levels induces oxidative stress, leading to structural and functional impairment of the kidneys. Cd uptake and MT induction can serve as useful environmental biomarkers.

Cd是一种不可降解的重金属污染物，没有已知的生物学作用。当被环境中的活生物体吸收时，会引起广泛的组织损伤。在这里，我们研究了暴露于20 mg / L ^-1 CdCl _2的0、24、48和72 h对海on Arius arius肾脏组织的影响。研究了镉的吸收，金属硫蛋白（MT）的诱导，微结构改变，DNA片段化和caspase-3活性。镉和MT水平是时间依赖性的并且是正相关的。鲍曼氏囊和小管的直径明显增加。同时，肾小球的密度，直径和体积以及肾小管的密度和体积降低。Cd通过提高caspase-3活性诱导细胞凋亡。这些结果支持以下观念：暴露于致死性Cd水平会诱发氧化应激，从而导致肾脏的结构和功能受损。镉吸收和MT诱导可作为有用的环境生物标志物。