Augmentation of chrysotile-induced oxidative stress by BHA in mice lungs

Our plain-English summary of Augmentation of chrysotile-induced oxidative stress by BHA in mice lungs, by I. Ahmad, K. Krishnamurthi, J.M. Arif, et al (Food and Chemical Toxicology, 1995).

The study

• Authors: I. Ahmad, K. Krishnamurthi, J.M. Arif, M. Ashquin, N. Mahmood, M. Athar, Q. Rahman
• Journal: Food and Chemical Toxicology
• Published: 1995;33(3):209-15
• Cited by: 7 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Abstract

Asbestos is known to induce oxidative stress in the lung. The consumption of butylated hydroxyanisole (BHA) in preserved food and soft drinks is increasing in the general population, which includes workers in asbestos factories. Because there is no information on the effect of co-exposure to chrysotile and BHA, the time-dependent effects of a single intratracheal dose of chrysotile (1 mg per mouse) and a single ip dose of BHA (350 mg/kg body weight) on various indices of oxidative stress such as lipid peroxidation, hydrogen peroxide generation, glutathione peroxidase (GPX), glutathione reductase (GR), catalase, glucose-6-phosphate dehydrogenase (G6PDH) and glutathione (GSH) were followed for up to 14 days. Microsomal lipid peroxidation (as well as that induced by NADPH) was significantly enhanced by BHA in the chrysotile-exposed group. GPX and GR activities in the same group were gradually decreased by BHA. Non-significant modulation of catalase activity by BHA was also noted. BHA induces GSH to a significant extent in lungs exposed with chrysotile. An increase in the G6PDH activity was maximal (19%; P < 0.05) at day 3. The results clearly demonstrate that BHA enhances chrysotile-induced oxidative stress in the lung.

In plain English

This animal experiment from Lucknow, India, tested whether the food preservative butylated hydroxyanisole (BHA) changes the oxidative stress that chrysotile asbestos causes in mouse lungs. Male mice, at least 16 per group, were divided into chrysotile, BHA, chrysotile plus BHA, and control groups. Chrysotile (1 mg per mouse) was placed once into the windpipe; BHA (350 mg/kg body weight) was injected once into the abdomen. Four mice per group were examined 1, 3, 7 and 14 days later. Compared with chrysotile alone, the combined group had more lipid peroxidation: 5% higher at day 1 and 42% higher at day 14. It also produced 74% more hydrogen peroxide at day 1. Glutathione peroxidase activity was 36% lower at day 3 and 21% lower afterwards. Glutathione reductase was 22% lower at day 14. Glutathione content was 38 to 56% higher throughout. Chrysotile alone significantly raised catalase compared with saline controls, by up to 62% at day 7, but adding BHA did not significantly change it. The authors concluded that BHA enhanced chrysotile-induced oxidative stress in the lung.

We wrote this plain-English summary from the full article with the help of AI, and a second AI model checked each sentence against the article. It is not the authors' wording; the abstract and the article are their own account.

What the study did and found

• Design: Animal experiment with four treatment groups followed over 14 days
• Who was studied: Male mice of about 20 g from the Industrial Toxicology Research Centre colony (Lucknow, India), at least 16 per group; four mice per group were killed at each of days 1, 3, 7 and 14
• Exposure: A single intratracheal dose of Indian chrysotile (1 mg in 0.2 ml saline per mouse) and/or a single intraperitoneal dose of BHA (350 mg/kg body weight in 0.1 ml corn oil); controls received vehicle
• Main results:
  • Compared with the chrysotile-only group, microsomal lipid peroxidation in the chrysotile plus BHA group was 5% higher at day 1 and 42% higher (P<0.01) at day 14
  • In chrysotile-exposed lungs at day 14, BHA enhanced NADPH-induced lipid peroxidation by 49% (P < 0.01) and iron-induced lipid peroxidation by 72% (P<0.001)
  • The co-exposure group produced 74% (P < 0.001) more hydrogen peroxide than the chrysotile group at day 1 and over 40% (P < 0.01) more on later days
  • Compared with the chrysotile group, glutathione peroxidase in the co-exposure group was 36% lower (P <0.001) at day 3 and 21% lower (P < 0.01) on the following days
  • Compared with chrysotile alone, co-exposure gradually lowered glutathione reductase activity, by 22% (P < 0.02) at day 14
  • Compared with saline controls, chrysotile alone gradually increased catalase activity, to a maximum of 62% (P < 0.01) at day 7, followed by 41% (P <0.01) at day 14
  • In the chrysotile-exposed group, BHA produced a non-significant increase in catalase until day 7 and a non-significant decrease at day 14
  • Compared with chrysotile alone, co-exposure raised G6PDH activity by 19% (P < 0.05) at day 3; at day 14 it was 9% lower (non-significant)
  • Glutathione content in the co-exposure group was significantly higher than in the chrysotile-only group (38-56%) throughout the observation period
  • In the chrysotile-only group, glutathione content gradually fell, by a maximum of 23% (P < 0.01) at day 14
• The authors' conclusion: The authors concluded that the increased lipid peroxidation and hydrogen peroxide generation, together with changes in antioxidant systems, indicate that BHA augments chrysotile-induced oxidative stress. They said the study provides experimental data relevant to BHA-associated risk in chrysotile-exposed people.

Topics

The National Library of Medicine indexes this study under subjects our site covers: Chrysotile.

Medical terms in this study, explained in our Lexicon: Chrysotile, Oxidative Stress, Glutathione (GSH).

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