Increase in rat plasma antioxidant activity after E. coli lipopolysaccharide administration

Area of Science:

• Toxicology
• Biochemistry
• Physiology

Background:

• Animal sensitivity to lipopolysaccharide (LPS) endotoxin varies significantly.
• Rats show increased hepatic endogenous antioxidative enzyme activity post-LPS administration.
• This hepatic response suggests a potential link to rat resistance to LPS.

Purpose of the Study:

• To investigate if the hepatic antioxidant system changes observed in rats after LPS administration occur systemically.
• To assess the impact of LPS on plasma antioxidant capacity (AOC) and cardiovascular parameters in rats.
• To determine the role of nitric oxide synthase in LPS-induced changes and rat resistance.

Main Methods:

• Male Sprague-Dawley and Wistar rats were administered varying doses of LPS (10-100 mg/kg) intraperitoneally under anesthesia.
• Plasma AOC, blood gas analysis, and cardiovascular parameters were measured over 4 hours.
• The effect of L-N(G)-Nitroarginine methyl ester hydrochloride (L-NAME), a nitric oxide synthase inhibitor, on LPS response was studied in Sprague-Dawley rats.

Main Results:

• High doses of LPS increased plasma AOC in rats during the early post-administration period.
• Both Sprague-Dawley and Wistar rats showed increased plasma AOC, but at different LPS doses reflecting their sensitivity.
• Pretreatment with L-NAME did not alter rat resistance to LPS or plasma AOC levels.

Conclusions:

• Rats, particularly Sprague-Dawley rats, display relative resistance to early toxic effects of LPS.
• Endotoxin-induced increases in plasma AOC may play a role in protecting rats against LPS intoxication.
• Nitric oxide synthase inhibition does not appear to influence the LPS-induced systemic antioxidant response or resistance in rats.