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Increasing evidence suggests that homeodomain-leucine zipper I (HD-Zip) I transcription factors play important roles in abiotic stress responses, but no HD-Zip I proteins have been reported in maize. Here, a drought-induced HD-Zip I gene, Zmhdz10, was isolated from maize and characterized for its role in stress responses. Real-time quantitative PCR showed that expression of Zmhdz10 was also induced by salt stress and ABA. Transient expression of Zmhdz10-green fluorescent protein (GFP) fusion proteins in onion cells showed a nuclear localization of Zmhdz10. Yeast hybrid assays demonstrated that Zmhdz10 has transactivation and DNA-binding activity in yeast cells. Overexpression of Zmhdz10 in rice led to enhanced tolerance to drought and salt stresses and increased sensitivity to ABA. Moreover, Zmhdz10 transgenic plants had lower relative electrolyte leakage (REL), lower malondialdehyde (MDA) and increased proline content relative to wild-type plants under stress conditions, which may contribute to enhanced stress tolerance. Zmhdz10 transgenic Arabidopsis plants also exhibited enhanced tolerance to drought and salt stresses that was concomitant with altered expression of stress/ABA-responsive genes, including Δ1-Pyrroline-5-carboxylate synthetase 1 (P5CS1), Responsive to dehydration 22 (RD22), Responsive to dehydration 29B (RD29B) and ABA-insensitive 1 (ABI1). Taken together, these results suggest that Zmhdz10 functions as a transcriptional regulator that can positively regulate drought and salt tolerance in plants through an ABA-dependent signaling pathway.

Recent studies have demonstrated nanosized titanium dioxide (nano-TiO2)-induced fertility reduction and ovary injury in animals. To better understand how nano-TiO2 act in mice, female mice were exposed to 2.5, 5, and 10 mg/kg nano-TiO2 by intragastric administration for 90 consecutive days; the ovary injuries, fertility, hormone levels, and inflammation-related or follicular atresia-related cytokine expression were investigated. The results showed that nano-TiO2 was deposited in the ovary, resulting in significant reduction of body weight, relative weight of ovary and fertility, alterations of hematological and serum parameters and sex hormone levels, atretic follicle increases, inflammation, and necrosis. Furthermore, nano-TiO2 exposure resulted in marked increases of insulin-like growth factor-binding protein 2, epidermal growth factor, tumor necrosis factor-α, tissue plasminogen activator, interleukin-1β, interleukin -6, Fas, and FasL expression, and significant decreases of insulin-like growth factor-1, luteinizing hormone receptor, inhibin α, and growth differentiation factor 9 expression in mouse ovary. These findings implied that fertility reduction and ovary injury of mice following exposure to nano-TiO2 may be associated with alteration of inflammation-related or follicular atresia-related cytokine expressions, and humans should take great caution when handling nano-TiO2.

Titanium dioxide nanoparticles (TiO2 NPs) are widely used in toothpastes, sunscreens, and products for cosmetic purpose that the human use daily. Although the neurotoxicity induced by TiO2 NPs has been demonstrated, very little is known about the molecular mechanisms underlying the brain cognition and behavioral injury. In this study, mice were exposed to 2.5, 5, and 10 mg/kg body weight (BW) TiO2 NPs by nasal administration for 90 consecutive days, respectively, and their brains' injuries and brain gene-expressed profile were investigated. Our findings showed that TiO2 NPs could be translocated and accumulated in brain, led to oxidative stress, overproliferation of all glial cells, tissue necrosis as well as hippocampal cell apoptosis. Furthermore, microarray data showed significant alterations in the expression of 249 known function genes, including 113 genes upregulation and 136 genes downregulation following exposure to 10 mg/kg BW TiO2 NPs, which were associated with oxidative stress, immune response, apoptosis, memory and learning, brain development, signal transduction, metabolic process, DNA repair, response to stimulus, and cellular process. Especially, significant increases in Col1a1, serine/threonine-protein kinase 1, Ctnnb1, cysteine-serine-rich nuclear protein-1, Ddit4, Cyp2e1, and Krev interaction trapped protein 1 (Krit1) expressions and great decreases in DA receptor D2, Neu1, Fc receptor-like molecules, and Dhcr7 expressions following long-term exposure to TiO2 NPs resulted in neurogenic disease states in mice. Therefore, these genes may be potential biomarkers of brain toxicity caused by TiO2 NPs exposure, and the application of TiO2 NPs should be carried out cautiously.