Selenium Protects against Lead-induced Apoptosis via Endoplasmic Reticulum Stress in Chicken Kidneys

Area of Science:

• Toxicology
• Nutritional Biochemistry
• Cell Biology

Background:

• Lead (Pb) is a toxic heavy metal known to induce apoptosis, a process of programmed cell death.
• Selenium (Se), an essential trace element, plays a crucial role in mitigating heavy metal toxicity.
• Endoplasmic reticulum (ER) stress is implicated in the cellular damage caused by toxic agents like lead.

Purpose of the Study:

• To investigate the alleviative effects of selenium on lead-induced apoptosis in chicken kidneys.
• To explore the role of endoplasmic reticulum (ER) stress in lead toxicity and selenium's protective mechanism.

Main Methods:

• 180 male chickens were divided into four groups, receiving different diets and drinking water with or without lead acetate and sodium selenite.
• Kidney tissues were collected on days 30, 60, and 90 for analysis of ultrastructure, nitric oxide (NO) content, and inducible nitric oxide synthase (iNOS) activity.
• Gene and protein expression of iNOS, ER-related genes (GRP78, GRP94, ATF4, ATF6, IRE), apoptosis markers (caspase-3, Bcl-2), and caspase-12 were quantified.

Main Results:

• Lead exposure altered kidney ultrastructure, decreased Bcl-2 expression, and increased NO content, iNOS activity, and expression of iNOS, ER-stress markers, caspase-3, and caspase-12.
• Selenium supplementation attenuated the detrimental effects of lead on kidney tissue and cellular markers.
• Lead-induced changes in NO content and specific ER and apoptosis-related gene expressions showed time-dependent patterns, which were mitigated by selenium.

Conclusions:

• Selenium effectively alleviates lead-induced apoptosis in chicken kidneys.
• Selenium protects against lead toxicity by reducing endoplasmic reticulum (ER) stress.
• The findings highlight the protective role of selenium against heavy metal-induced cellular damage in poultry.