Amelioration of Aluminium Toxicity in Pigeon Pea [Cajanus cajan (L.) Millsp.] Plant by 24-Epibrassinolide

The effect of 24-epibrassinolide on growth of pigeon pea [Cajanus cajan (L.) Millsp.] under aluminium toxicity was studied. 24-EBL reduced the impact of Al stress on plant growth. Particularly 24-EBL reduced the inhibitory impact of aluminium toxicity on root growth which was further manifested in overall improvement of vegetative growth. Application of 24-epibrassinolide removed the inhibitory influence of Al nodulation. The growth stimulation in Cajanus plants by 24-EBL under Al stress was associated with elevated levels of chlorophylls, nucleic acids and soluble proteins. 24-Epibrassinolide application enhanced proline content in Al3+ stressed Cajanus plants. Further, the supplementation of 24-epibrassinolide to Al stress treatments increased the activities of antioxidative enzymes viz., catalase [EC 1.11.1.6];peroxidase [EC 1.11.1.7];superoxide dismutase [EC 1.15.1.1] and ascorbate peroxidase [EC 1.11.1.11]. Lipid peroxidation induced by Al was found reduced with the supplementation of 24-epibrassinolide. The present studies demonstrated the ameliorating capability of 24-epibrassinolide on the Al induced inhibition of plant growth of C. cajan.

α-Linolenic acid alleviates aluminium chloride-induced toxicity in PC12 cells by activation of PKA-CREB-BDNF signaling pathway

Aluminum has been associated with neurodegenerative diseases.ALA(α-linolenic acid),an essential dietary component for human health,possesses prominent biological activities.Herein,we aim to explore the neuroprotective effects of ALA on aluminum toxicity and reveal the underlying mechanism.Results show that aluminum chloride(denoted as Al)enabled cell viability decline and apoptosis with oxidative stress and mitochondrial damage in differentiated rat pheochromocytoma cells(PC12)for 24 h incubation.Compared with Al(10 mmol/L)treatment alone,ALA(50μmol/L)pretreatment for 24 h significantly enhanced cell viability by 28.40%,and hindered cell apoptosis by 12.35%,together with recovering redox state balance and alleviating mitochondrial damage.It was measured that ALA treatment upregulated Bcl-2 expression and down-regulated Bax level,accompanied with an expression decline of caspase-3 and caspase-9.Meanwhile,ALA pretreatment was proved to increase protein kinase A(PKA)expression and to promote phosphorylation of cAMP response element-binding protein(p-CREB),resulting in elevation on the level of brain-derived neurotrophic factor(BDNF).The above results showed that ALA attenuated Al toxicity in PC12 cells by mediating the PKA-CREBBDNF signaling pathway.

Acute Toxicity of Aluminium Phosphide Following Oral Administration in Rats

Aluminium phosphide (AlP) is used as a fumigant and also sometimes misused for suicidal attempts in India, due to its easy availability. The effect of phosphine, the gas that is liberated when AlP comes in contact with moisture, is well documented in the literature. However, the effect of AlP in its native form on animal models is not well cited. In this study we examined the acute toxic effect of AlP in rats. Oral LD50 of AlP for male and female rats were found to be 14. 13 and 11. 89mg/kg, respectively. Oral administration of an AlP dose of 0. 80 LD50 resulted in significant increases in the level of plasma glutamic oxaloacetic transaminase,alkaline phosphatase, glucose and urea in rats of both sexes. Hemoglobin level and packed cell volume also increased significantly 6h after administration. Body weight was reduced but the organ to body weight ratio of lung, liver, spleen, kidney and testes remained unchanged.Histopathological changes induced by AlP during 24-48h induced hemorrhage, congestion and mild to moderate atrophy of various cellular components of visceral organs. The study showed that the acute toxic effect of AlP may be due to hypovolemic shock. Female rats were found to be more susceptible than were males.