Genotoxic effects of caffeine in female mice exposed during pregnancy and lactation period and their offspring.

Caffeine is a widely consumed substance, and there is a discussion about its effects when ingested by women during pregnancy and lactation. We aimed to identify the genotoxic effects of caffeine in female mice that consumed it during pregnancy and lactation periods and its consequences in their offspring. Thirty-six couples of Swiss mice received water or caffeine (0.3 and 1.0 mg/mL) treatment during pregnancy and lactation. The male and female offspring were divided into 12 groups according to the treatment administered to the female mice. Genotoxicity was assessed using the comet assay and the micronucleus test. Both doses of caffeine showed genotoxic effects in pregnant and lactating mice groups compared to groups not administered caffeine. In relation to offspring, it can be observed that females and males of the offspring had low weight in early life. In both female and male offspring, genotoxicity was detected in the blood, liver, and kidney tissues. Thus, from the present study, we can suggest that the caffeine consumed by female mice during the periods of pregnancy and lactation led to genotoxic effects in their offspring.

Anti-genotoxic and anti-mutagenic effects of melatonin supplementation in a mouse model of melanoma.

Melanoma, an aggressive skin cancer originating from melanocytes, can metastasize to the lungs, liver, cortex, femur, and spinal cord, ultimately resulting in DNA mutagenic effects. Melatonin is an endogenous hormone and free radical scavenger that possesses the ability to protect the DNA and to exert anti-proliferative effects in melanoma cells. The aim of this study was to evaluate the effects of B16F10 melanoma cells and the effects of melatonin supplementation on genotoxic parameters in murine melanoma models. Thirty-two male C57Bl/6 mice were divided in the following four groups: PBS + vehicle (n = 6), melanoma + vehicle (n = 10), PBS + melatonin (n = 6), and melanoma + melatonin (n = 10). The melanoma groups received a B16F10 cell injection, and melatonin was administered during 60 days. After treatment, tumor sizes were evaluated. DNA damage within the peripheral blood, lungs, liver, cortex, and spinal cord was determined using comet assay, and the mutagenicity within the bone marrow was determined using the micronucleus test. B16F10 cells effectively induced DNA damage in all tissues, and melatonin supplementation decreased DNA damage in the blood, liver, cortex, and spinal cord. This hormone exerts anti-tumor activity via its anti-proliferative, antioxidative, and pro-apoptotic effects. As this result was not observed within the lungs, we hypothesized that melatonin can induce apoptosis in cancer cells, and this was not evaluated by comet assay. This study provides evidence that melatonin can reduce the genotoxicity and mutagenicity caused by B16F10 cells.