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IntroductionLead (Pb) has many applications in daily life, but in recent years, various problems caused by lead exposure have aroused people’s concern. Folic acid is widely found in fruits and has received more attention for its antioxidant function. However, the role of folic acid in lead-induced kidney injury in rats is unclear. This study was designed to investigate the effects of folic acid on oxidative stress and endoplasmic reticulum stress in the kidney of rats caused by lead exposure.MethodsForty specific pathogen-free male Rattus norvegicus rats were randomly divided into control, lead, intervention, and folic acid groups. The levels of SOD, GSH-Px, GSH, and MDA were measured by biochemical kits. The protein levels of Nrf2, HO-1, CHOP, and GRP78 were measured by immunofluorescence.ResultsThis study showed that lead exposure increased the blood levels of lead in mice. However, the intervention of folic acid decreased the levels of lead, but the difference was not statistically significant. Lead exposure causes oxidative stress by decreasing kidney SOD, GSH-Px, and GSH levels and increasing MDA levels. However, folic acid alleviated the oxidative damage caused by lead exposure by increasing the levels of GSH-Px and GSH and decreasing the levels of MDA. Immunofluorescence results showed that folic acid intervention downregulated the upregulation of kidney Nrf2, HO-1, GRP78, and CHOP expression caused by lead exposure.DiscussionOverall, folic acid alleviates kidney oxidative stress induced by lead exposure by regulating Nrf2 and HO-1, while regulating CHOP and GRP78 to mitigate apoptosis caused by excessive endoplasmic reticulum stress.

BackgroundLead poisoning causes an oxidative stress response – a key “bridge” connecting various pathways – in the human body. Oxidative stress usually implies an imbalance between pro-oxidants and antioxidants. Moreover, Nrf2, Keap1, and TXNIP proteins play an essential role in oxidative stress. Some studies showed that pea peptides could alleviate the oxidative stress response. However, the effect and mechanism of pea peptide on oxidative stress response induced by lead in PC12 cells has not been reported.AimInvestigating the effect and mechanism of pea peptides in alleviating oxidative damage in PC12 cells induced by lead.MethodsIn this study, cell viability was measured by CCK8 (Cell Counting Kit-8). Superoxide dismutase (SOD), catalase (CAT), glutathione (GSH), glutathione reductase (GR), glutathione peroxidase (GPx), reactive oxygen species (ROS), and lipid peroxidation (MDA) were measured using the corresponding Biochemical kits. The Keap1, Nrf2, and TXNIP protein expressions were tested using Western blot.ResultsPea peptides PP3, PP4, and PP6 could reverse the decrease of cell viability caused by lead exposure (P < 0.05), the elevation of ROS and MDA caused by lead exposure, and the decrease of CAT, SOD, GR, GPx, and GSH/GSSG caused by lead exposure (P < 0.05). Moreover, PP3, PP4, and PP6 could reduce the elevated expression of Keap1 and TXNIP caused by lead exposure; and increase the expression of Nrf2 (P < 0.05).ConclusionPP3, PP4, and PP6 can alleviate lead-induced oxidative stress damage in PC12 cells, and the Nrf2/Keap1/TXNIP signaling pathway may play an essential role in this process.