Iron deficiency and cognitive impairment in children with low blood lead levels

Maidoumi, Sana; Ouaziz, Charif Radouan; Ouisselsat, Mariam; Maouaki, Amal El; Loukid, Mohamed; Lekouch, Nadra; Pineau, Alain; Ahami, Ahmed Omar Touhami; Sedki, A.

doi:10.1016/j.toxrep.2022.08.008

Cited by 4 publications

(1 citation statement)

References 39 publications

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“…Due to the non-biodegradable nature of Pb 2+ , it can accumulate in soil, rivers, lakes, and air, which are the main sources of Pb 2+ exposure for humans. The World Health Organization established that there is no safe concentration of Pb 2+ in the blood, as even a low amount of Pb 2+ has been related to cognitive impairment, particularly in children [4][5][6]. This heavy metal can enter the organism by ingestion, inhalation, and absorption, and once inside, it is distributed to the organs and stored in the teeth and bones [7][8][9][10][11][12].…”

Section: Introductionmentioning

confidence: 99%

Modulation of Kynurenic Acid Production by N-acetylcysteine Prevents Cognitive Impairment in Adulthood Induced by Lead Exposure during Lactation in Mice

Ovalle Rodríguez,

Ramírez Ortega,

Blanco Ayala

et al. 2023

Antioxidants

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Lead (Pb2+) exposure during early life induces cognitive impairment, which was recently associated with an increase in brain kynurenic acid (KYNA), an antagonist of NMDA and alpha-7 nicotinic receptors. It has been described that N-acetylcysteine (NAC) favors an antioxidant environment and inhibits kynurenine aminotransferase II activity (KAT II, the main enzyme of KYNA production), leading to brain KYNA levels decrease and cognitive improvement. This study aimed to investigate whether the NAC modulation of the brain KYNA levels in mice ameliorated Pb2+-induced cognitive impairment. The dams were divided into four groups: Control, Pb2+, NAC, and Pb2++NAC, which were given drinking water or 500 ppm lead acetate in the drinking water ad libitum, from 0 to 23 postnatal days (PNDs). The NAC and Pb2++NAC groups were simultaneously fed NAC (350 mg/day) in their chow from 0 to 23 PNDs. At PND 60, the effect of the treatment with Pb2+ and in combination with NAC on learning and memory performance was evaluated. Immediately after behavioral evaluation, brain tissues were collected to assess the redox environment; KYNA and glutamate levels; and KAT II activity. The NAC treatment prevented the long-term memory deficit exhibited in the Pb2+ group. As expected, Pb2+ group showed redox environment alterations, fluctuations in glutamate levels, and an increase in KYNA levels, which were partially avoided by NAC co-administration. These results confirmed that the excessive KYNA levels induced by Pb2+ were involved in the onset of cognitive impairment and could be successfully prevented by NAC treatment. NAC could be a tool for testing in scenarios in which KYNA levels are associated with the induction of cognitive impairment.

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