Lactobacillus brevis BIOTECH 1766 Attenuates Oxidative Stress and Histopathological Changes following Aluminum Poisoning in ICR Mice

Abstract

Objective. The aim of this study was to investigate the protective effects of Lactobacillus brevis BIOTECH 1766
against oxidative damage in the brain, liver, and kidneys induced by aluminum (Al) poisoning in ICR mice.

Methods. Twenty mice were divided into four groups (n = 5): (I) control, (II) Al, (III) citric acid (CA), and (IV) L. brevis BIOTECH 1766 group. A 14-day treatment period was implemented, wherein groups I and II received sterile water, while groups III and IV received 10 mg/kg bw of CA and 1 x 109 cfu/kg bw of L. brevis BIOTECH 1766, respectively. On day 15, all except the control group received a single oral dose of 1438 mg/kg bw of AlCl3
. 6H2O. After 24 h, mice were euthanized to collect the brain, liver, and kidneys for the oxidative stress marker analyses and histopathological examination.

Results. Acute intoxication of Al led to a significant increase in tissue malondialdehyde (MDA) and a significant
decrease in the tissue's reduced glutathione (GSH), catalase (CAT), and superoxide dismutase (SOD). Mice pretreated with CA or L. brevis BIOTECH 1766 have markedly reduced CAT activity in the liver, and SOD in all three organs. Extensive organ injuries were also prevented by CA and L. brevis BIOTECH 1766 pretreatment, with the latter providing better protection against liver damage.

Conclusion. The findings showed that L. brevis BIOTECH 1766 provides a protective effect against acute Al
poisoning in mice by ameliorating oxidative damage in the brain, liver, and kidneys.