Evaluation and Identification of Promising Introgression Lines Derived From Wild Cajanus Species for Broadening the Genetic Base of Cultivated Pigeonpea [Cajanus cajan (L.) Millsp.].

Pigeonpea [Cajanus cajan (L.) Millsp.], a multipurpose and nutritious grain legume crop, is cultivated for its protein-rich seeds mainly in South Asia and Eastern and Southern Africa. In spite of large breeding efforts for pigeonpea improvement in India and elsewhere, genetic enhancement is inadequate largely due to its narrow genetic base and crop susceptibility to stresses. Wild Cajanus species are novel source of genetic variations for the genetic upgradation of pigeonpea cultivars. In the present study, 75 introgression lines (ILs), derived from crosses involving cultivated pigeonpea variety ICPL 87119 and wild Cajanus cajanifolius and Cajanus acutifolius from the secondary gene pool, were evaluated for yield and yield-attributing traits in diverse environments across locations and years. Restricted maximum likelihood (REML) analysis revealed large genetic variations for days to 50% flower, days to maturity, plant height, primary branches per plant, pods per plant, pod weight per plant, 100-seed weight, and grain yield per plant. Superior ILs with mid-early to medium maturity duration identified in this study are useful genetic resources for use in pigeonpea breeding. Additive main effects and multiplicative interaction (AMMI) analysis unfolded large influence of environment and genotype × environment interaction for variations in yield. A few lines such as ICPL 15023 and ICPL 15072 with yield stability were identified, while a number of lines were completely resistant (0%) to sterility mosaic diseases and/or Fusarium wilt. These lines are novel genetic resources for broadening the genetic base of pigeonpea and bring yield stability and stress tolerance. High-yielding lines ICPL 15010, ICPL 15062, and ICPL 15072 have been included in the initial varietal trials (IVTs) of the All India Coordinated Research Project (AICRP) on pigeonpea for wider evaluation across different agro-ecological zones in India for possible release as variety(ies).

Oxidative stress and inflammatory responses of rat following acute inhalation exposure to iron oxide nanoparticles.

In this research, we investigated the toxicity responses of rat following a continuous 4 h inhalation exposure of only the head and nose to iron oxide nanoparticles (Fe(3)O(4) NPs, size = 15-20 nm). The rats for the investigation were exposed to a concentration of 640 mg/m(3) Fe(3)O(4) NPs. Markers of lung injury and proinflammatory cytokines (interleukin-1ß, tumor necrosis factor-α, and interleukin-6) in bronchoalveolar lavage fluid (BALF) and blood, oxidative stress in lungs, and histopathology were assessed on 24 h, 48 h, and 14 days of postexposure periods. Our results showed a significant decrease in the cell viability, with the increase in the levels of lactate dehydrogenase, total protein, and alkaline phosphatase in the BALF. Total leukocyte count and the percentage of neutrophils in BALF increased within 24 h of postexposure. Immediately following acute exposure, rats showed increased inflammation with significantly higher levels of lavage and blood proinflammatory cytokines and were consistent throughout the observation period. Fe(3)O(4) NPs exposure markedly increased malondialdehyde concentration, while intracellular reduced glutathione and antioxidant enzyme activities were significantly decreased in lung tissue within 24-h postexposure period. On histological observation, the lung showed an early activation of pulmonary clearance and a size-dependant biphasic nature of the Fe(3)O(4) NPs in causing the structural alteration. Collectively, our data illustrate that Fe(3)O(4) NPs inhalation exposure may induce cytotoxicity via oxidative stress and lead to biphasic inflammatory responses in Wistar rat.

Acute inhalation toxicity of cerium oxide nanoparticles in rats.

The aim of the present study was to assess the acute toxic potential of cerium oxide nanoparticles (CeO(2) NPs) in rats when exposed through the head and nose inhalation route. The rats were exposed to CeO(2) NPs and the resultant effects if any, to cause cytotoxicity, oxidative stress and inflammation in the lungs were evaluated on a 24h, 48h and 14 day post exposure period. Our results showed a significant decrease in the cell viability, with the increase of lactate dehydogenase, total protein and alkaline phosphatase levels in the bronchoalveolar lavage fluid (BALF) of the exposed rats. Total leukocyte count and the percentage of neutrophils in BALF were elevated within 24h of post exposure. The concentrations of pro-inflammatory cytokines (IL-1ß, TNF-α, and IL-6) were significantly increased in the BALF and in the blood throughout the observation period. The level of malondialdehyde was elevated with the decreased levels of intracellular reduced glutathione (GSH) in the lung after exposure. The alveolar macrophages (AMs) and neutrophils overloaded with phagocytosed CeO(2) NPs were observed along with non-phagocytosed free CeO(2) NPs that were deposited over the epithelial surfaces of the bronchi, bronchiole and alveolar regions of lungs within 24h of post exposure and were consistent throughout the observation period. A well distributed, multifocal pulmonary microgranulomas due to impairment of clearance mechanism leading to biopersistence of CeO(2) NPs for an extended period of time were observed at the end of the 14 day post exposure period. These results suggest that acute exposure of CeO(2) NPs through inhalation route may induce cytotoxicity via oxidative stress and may lead to a chronic inflammatory response.