Long-term Effects Of Continuous Exposure Research Articles

Effects of Long-Term Exposure to Low-Power 915 MHz Unmodulated Radiation on Phaseolus vulgaris L.

The morphophysiological response of Phaseolus vulgaris L. to low-power electromagnetic radiation was investigated in order to assess the potential harmful effects of long-term continuous exposure. The plants were grown in two separate electromagnetic field (EMF) shielded rooms, in a controlled, greenhouse-like environment. One batch was continuously irradiated during the growth period (from sowing to maturity) and the other one was used as a reference. An unmodulated signal at 915 MHz (the central frequency between the uplink and downlink of the GSM900 mobile communications band) was used, with a maximum power density of 10 mW/m2 measured near the plants. The plants were analyzed using ultraviolet-visible, statistical, morphometric, and electron microscopy methods. Significant differences were observed regarding the height of the plants, number of inflorescences, and chlorophyll and carotenoid content, all closely connected with the ultrastructural changes observed in the leaves. The irradiated batch grew higher (19% increase in plant height, 20% increase in stem and leaves' dry mass), with 18% fewer inflorescences, and extremely long roots (34% increase in dry mass). The ultrastructure of the irradiated leaves showed irregular cells and a higher content of plastoglobules in the chloroplasts. All results indicate that the irradiated plants suffered significant morphological modifications during their long-term exposure to the specific EM radiation. Bioelectromagnetics. © 2020 Bioelectromagnetics Society.

Induction of oxidative stress and DNA damage in rat brain by a folate/methyl-deficient diet

The age-associated decline in cellular antioxidant defenses and resultant accumulation of DNA damage in central nervous system has been mechanistically implicated in the etiology and pathogenesis of neurodegenerative diseases. Neurons possess a high metabolic activity and are especially vulnerable to the long-term effects of continuous exposure to endogenous reactive oxygen species. It is well recognized that adequate availability of essential nutrients involved in cellular one-carbon metabolism is essential for normal brain development and function. Additionally, the synthesis of the primary low-molecular cellular antioxidant glutathione is inter-dependently linked to one-carbon metabolic pathway. Thus, any aberrant disruptions in one-carbon metabolism can result in potentially deleterious effects including cell death as a result of an imbalance in the cellular redox state. Hence, in the present study, we examined the long-term effects of a folate/methyl-deficient (FMD) diet on cellular antioxidant defenses and DNA damage in the rat brain. Feeding male Fisher 344 rats a FMD diet resulted in perturbations in the levels of one-carbon metabolites along with induction of oxidative stress and oxidative DNA damage in the brain. This was evidenced by a decrease in the reduced oxidized/glutathione ratio, imbalance of cellular antioxidant defense system; specifically, altered activity and expression of antioxidant enzymes Mn-containing superoxide dismutase (Mn-SOD), catalase, and glutathione peroxidase (GPX), increased accumulation of oxidative DNA lesions, 8-hydroxydeoxyguanosine (8-OH-dG) and DNA single-strand breaks, even in the presence of increased expression of critical DNA repair genes apurinic/apyrimidinic endonuclease 1 ( Apex1) and DNA polymerase beta ( Polβ), and apoptosis in the brains of folate/methyl-deficient rats. These results indicate that chronic methyl group deficiency leads to an imbalance in cellular antioxidant defense systems, increased oxidative stress, and apoptosis. Any of these events may compromise normal central nervous system function and contribute to the development of various neurological, behavioral, and neurocognitive dysfunctions.

Effects of long-term continuous exposure to light on memory and anxiety in mice

The studies on the relationship between the light/dark cycle and memory function mostly used protocols of acute disruption of the circadian rhythm. The aim of the present study is to verify the effects of long-term continuous exposure to light on memory, anxiety and motor parameters of mice tested in the plus-maze discriminative avoidance task. Mice were conditioned to choose between the two enclosed arms (one aversive and one non-aversive) while avoiding the open arms of a modified elevated plus-maze apparatus. Memory was evaluated by the time spent in the aversive enclosed arm, anxiety was evaluated by the time spent in the open arms and locomotor behavior was evaluated by number of entries in the arms of the maze. The results showed that long-term (35–42 days) continuous light exposure did not modify memory or anxiety parameters but increased locomotor activity. While the increase in locomotor behavior is in line with previous studies, the unexpected absence of alterations in memory and anxiety (reported to be influenced by the circadian rhythm) is discussed.

Effects of continuous exposure to light on behavioral dopaminergic supersensitivity

Background: This study examines the effects of long-term continuous exposure to light on dopaminergic supersensitivity induced by repeated treatment with haloperidol in rats.Methods: Spontaneous general activity in an open-field (SGA) and stereotyped behavior induced by apomorphine (SB-APO) or amphetamine (SB-AMP) were used as experimental parameters. Rats were allocated to four groups in each experiment: saline-treated animals kept under a 12-hour light/dark cycle (LD) or 24-hour light/light cycle (LL), and 2 mg/kg haloperidol-treated animals kept under the above cycles. Plasma corticosterone concentration was also measured by radioimunoassay in saline-treated rats kept under a LD or LL cycle.Results: All the behavioral parameters used showed the development of central dopaminergic supersensitivity in rats kept under both cycles. Continuous exposure to light enhanced SGA and SB-AMP in both saline- and haloperidol-treated rats, but did not modify SB-APO. Animals kept under the LL cycle presented an increased plasma corticosterone concentration.Conclusions: Our results suggest that continuous exposure to light leads to an increase in dopaminergic function in both normal and “supersensitive” rats. This effect seems to be mediated by a presynaptic mechanism possibly involving corticosterone actions.

Long-term effects of continuous exposure to amphetamine on brain dopamine concentration and synaptosomal uptake in mice

Continuous release of p-chloroamphetamine from subcutaneously implanted minipumps for 3 days decreased brain 5-hydroxytryptamine, but not norepintamine or dopamine, when analyzed 2 weeks later. In contrast, 2 weeks after infusion of amphetamine, whole brain dopamine but not 5-hydroxytryptamine or norepinephrine, was decreased. Also, the high affinity uptake of [ 3H]dopamine was markedly and selectively reduced in striatal synaptosomes. Thus, neurotoxicity is apparently not unique to halogenated amphetamine derivatives, but is produced by amphetamine itself if administered continuously.

Long-term effects of continuous exposure to p-chloroamphetamine on central serotonergic mechanisms in mice

Consistent with its effects in rats, the i.p. administration of 45 mg/kg of p-chloroamphetamine (PCA) to mice produced decreases in brain levels of 5-hydroxytryptamine (5-HT), 5-hydroxyindoleacetic acid and tryptophan hydroxylase activity at early times after its administration. However, in contrast to the long-lasting nature of these reductions in rats, substantial recovery was evident within 2 weeks in mice. Regional analyses indicated that the hippocampus and remaining telencephalon were most sensitive to the PCA-induced decrease in 5-HT levels; however, complete recovery was observed 1 month after the administration of 45 mg/kg of PCA even in these relatively sensitive areas. These data are consistent with previous results indicating that PCA does not produce long-term, neurotoxic effects on serotonergic neurons in mice. However, the continuous release of PCA from subcutaneously implanted ALZET Osmotic Minipumps for a period of 3 days produced decreases in brain levels of 5-HT which lasted for at least 4 weeks. This finding suggests that the insensitivity of mice to the neurotoxic effects of PCA is related to its relatively short half-life in this species.