The influence of soman on the expression of tp53 gene in the rat brain; distant effect

• Autorzy: Brytan M. , Kowalczyk M. , Lapot M. , Paruszewska E. , Antkowiak B. , Przekop F. , Ciechanowska M.
• Języki publikacji: EN

Abstrakty

EN

INTRODUCTION: The organophosphorus compound soman (GD), an irreversible inhibitor of cholinesterases, produces seizure activity and related brain damage. Studies using various biochemical markers of programmed cell death indicate apoptotic rather than necrotic mechanism of GD-induced acute cell damage in the brain. One of the most important links between the proliferation and cell death machinery is the tumor suppressor p53, which as a guardian of the genome and the element promoting apoptosis makes it a prime target for a prognostic factor. AIM(S): The aim of this study was to examine distant effects of poisoning with a small, repeated dose of GD on the expression of mRNA encoding p53 protein in the rat brain. METHOD(S): The study was performed on maternal generation (F0) and on first filial generation (F1) of Wistar rats. Low clinically asymptomatic dose of GD (0.2×LD50) was administered by subcutaneous repeated injections, first in pregnancy and subsequently during the lactation period. Six months after the end of poisoning the animals were euthanised and brain structures (hippocampus, cerebellum and piriform cortex) were isolated aseptically for evaluation of p53 mRNA. To determine p53 transcript levels Real-Time PCR with SYBR Green dye was applied. RESULTS: GD action resulted in a significant increase of p53 transcript in the cerebellum and in the piriform cortex of both F0 and F1 females as well as in F1 males. The significant elevation of p53 mRNA level in the hippocampus was observed only in F1 females. CONCLUSIONS: The study demonstrates that GD causes distant changes in the expression of p53 mRNA in the rat brain. Increased expression of p53 mRNA provides indirect evidence that GD-induced distant disorders may include DNA damage and cell cycle disturbances leading to cell dysfunction and their elimination via apoptosis. FINANCIAL SUPPORT: This work was supported by Polish Ministry of Science and Higher Education No O R00 0042 08, “Soldier as a precise weapon – individual sets and kits”.

• Wydawca: -
• Czasopismo: Acta Neurobiologiae Experimentalis
• Rocznik: 2017
• Tom: 77
• Numer: Suppl.1
• Opis fizyczny: p.109

Twórcy

autor

Brytan M.

• Department of Pharmacology and Toxicology, The Karol Kaczkowski Military Institute of Hygiene and Epidemiology, Warsaw, Poland

autor

Kowalczyk M.

• Department of Pharmacology and Toxicology, The Karol Kaczkowski Military Institute of Hygiene and Epidemiology, Warsaw, Poland
• Josef Pilsudski University of Physical Education, Warsaw, Poland

autor

Lapot M.

• Department of Pharmacology and Toxicology, The Karol Kaczkowski Military Institute of Hygiene and Epidemiology, Warsaw, Poland

autor

Paruszewska E.

• Department of Pharmacology and Toxicology, The Karol Kaczkowski Military Institute of Hygiene and Epidemiology, Warsaw, Poland

autor

Antkowiak B.

• Department of Pharmacology and Toxicology, The Karol Kaczkowski Military Institute of Hygiene and Epidemiology, Warsaw, Poland

autor

Przekop F.

• The Kielanowski Institute of Animal Physiology and Nutrition Polish Academy of Sciences, Jablonna, Poland

autor

Ciechanowska M.

• Department of Pharmacology and Toxicology, The Karol Kaczkowski Military Institute of Hygiene and Epidemiology, Warsaw, Poland