Chronic pulmonary exposure to traffic-related fine particulate matter causes brain impairment in adult rats.

BACKGROUND: Effects of air pollution on neurotoxicity and behavioral alterations have been reported. The objective of this study was to investigate the pathophysiology caused by particulate matter (PM) in the brain. We examined the effects of traffic-related particulate matter with an aerodynamic diameter of < 1 µm (PM1), high-efficiency particulate air (HEPA)-filtered air, and clean air on the brain structure, behavioral changes, brainwaves, and bioreactivity of the brain (cortex, cerebellum, and hippocampus), olfactory bulb, and serum after 3 and 6 months of whole-body exposure in 6-month-old Sprague Dawley rats. RESULTS: The rats were exposed to 16.3 ± 8.2 (4.7~ 68.8) µg/m3 of PM1 during the study period. An MRI analysis showed that whole-brain and hippocampal volumes increased with 3 and 6 months of PM1 exposure. A short-term memory deficiency occurred with 3 months of exposure to PM1 as determined by a novel object recognition (NOR) task, but there were no significant changes in motor functions. There were no changes in frequency bands or multiscale entropy of brainwaves. Exposure to 3 months of PM1 increased 8-isoporstance in the cortex, cerebellum, and hippocampus as well as hippocampal inflammation (interleukin (IL)-6), but not in the olfactory bulb. Systemic CCL11 (at 3 and 6 months) and IL-4 (at 6 months) increased after PM1 exposure. Light chain 3 (LC3) expression increased in the hippocampus after 6 months of exposure. Spongiosis and neuronal shrinkage were observed in the cortex, cerebellum, and hippocampus (neuronal shrinkage) after exposure to air pollution. Additionally, microabscesses were observed in the cortex after 6 months of PM1 exposure. CONCLUSIONS: Our study first observed cerebral edema and brain impairment in adult rats after chronic exposure to traffic-related air pollution.

Sweet potato calmodulin SPCAM is involved in salt stress-mediated leaf senescence, H2O2 elevation and senescence-associated gene expression.

The sweet potato calmodulin gene, SPCAM, was previously cloned and shown to participate in ethephon-mediated leaf senescence, H2O2 elevation and senescence-associated gene expression. In this report, an association of SPCAM with NaCl stress is reported. Expression of SPCAM was significantly enhanced by NaCl on days 1 and 2 after salt treatment in a dose-dependent manner and drastically decreased again on the third day. Starting on day 6, salt stress also remarkably promoted leaf senescence, H2O2 elevation and senescence-associated gene expression in a dose-dependent manner. These salt stress-mediated effects were strongly inhibited by chlorpromazine, a calmodulin inhibitor, and the chlorpromazine-induced repression could be reversed by exogenous application of purified calmodulin fusion protein. These data suggest an involvement of calmodulin in salt stress-mediated leaf senescence, H2O2 elevation and senescence-associated gene expression in sweet potato. Exogenous application of SPCAM fusion protein alone, however, did not significantly accelerate leaf senescence and senescence-associated gene expression, but only showed a slight effect 12 days after treatment. These data suggest that additional components are involved in salt stress-mediated leaf senescence in sweet potato, possibly induced by and coordinated with SPCAM. In conclusion, the sweet potato calmodulin gene is NaCl-inducible and participates in salt stress-mediated leaf senescence, H2O2 elevation and senescence-associated gene expression.

Cloning and characterization of a sweet potato calmodulin SPCAM that participates in ethephon-mediated leaf senescence, H2O2 elevation and senescence-associated gene expression.

In this report a full-length cDNA, SPCAM, was isolated from ethephon-treated mature leaves of sweet potato. SPCAM contained 450 nucleotides (149 amino acids) in its open reading frame, and exhibited high amino acid sequence identities (ca. 76-100%) with several plant calmodulins, including Arabidopsis, carrot, ghost needle weed, pea, potato, soybean, sweet chestnut, and tobacco. Sweet potato SPCAM also contained four putative conserved calmodulin EF-hand motifs, which responded for Ca(2+) binding and cellular signalling. Phylogenetic tree analysis showed that sweet potato SPCAM exhibited closely-related association with Arabidopsis AtCAM7, which functioned as a transcriptional regulator. Reverse transcription-polymerase chain reaction (RT-PCR) analysis showed that SPCAM gene expression was not significantly increased from L1 immature leaf to L3 mature leaf, however, was remarkably enhanced in L4 early senescent leaf, and then decreased in L5 late senescent leaf. In dark- and ethephon-treated mature leaves, SPCAM expression was significantly increased from 6 to 48h, then decreased gradually until 72h after treatment. Ethephon-mediated leaf senescence, H(2)O(2) elevation, and senescence-associated gene expression, however, was remarkably inhibited by chlorpromazine, a calmodulin inhibitor. Exogenous application of purified calmodulin SPCAM fusion protein reversed the chlorpromazine repression of ethephon-mediated leaf senescence, H(2)O(2) elevation and senescence-associated gene expression. Based on these data we conclude that sweet potato SPCAM is an ethephon-inducible calmodulin and its expression is enhanced in natural and induced senescent leaves. Calmodulin SPCAM may play a physiological role in ethephon-mediated leaf senescence, H(2)O(2) elevation and senescence-associated gene expression in sweet potato leaves.