No influence of beta‐carotene on smoking‐induced dna damage as reflected by sister chromatid exchanges

The putative cancer‐preventive potential of β‐carotene may be explained by its anti‐oxidant capacity to prevent free‐radicalinduced DNA damage. To evaluate this hypothesis, we studied the effect of 14 weeks of β‐carotene supplementation on the frequency of sister chromatid exchanges (SCE) in lymphocytes in 143 heavy smokers in a randomized, double‐blind, placebocontrolled intervention trial. Age, smoking habits and pretreatment blood levels of cotinine, β‐carotene, retinol and vitamins C and E were similar in the placebo group (n = 73) and the treatment group (n = 70). Plasma β‐carotene levels increased 13‐fold in the treatment group during intervention, whereas the other parameters remained stable in both groups. Initial SCE levels were similar in the treatment and placebo groups (5.10 ± 0.98 vs. 5.00 ± 0.99 SCE/lymphocyte). During the intervention, both groups showed an almost identical decrease, and at the end of the intervention period there was no difference in SCE levels between the treatment and the placebo groups (4.37 ± 0.38 vs. 4.24 ± 0.37 SCE/lymphocyte). This study shows no protective effect of β‐carotene on DNA damage as reflected by sister chromatid exchanges in lymphocytes. Our results thus do not yield support for a cancerpreventive mechanism of β‐carotene involving this form of DNA damage. It cannot be excluded, however, that β‐carotene prevents other forms of smoking‐induced DNA damage, affects other tissues, or is preventive in later stages of carcinogenesis.