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Oral exposure to chromium hexavalent [Cr(VI)] has disastrous impacts and affects many people worldwide. Cr(VI) triggers neurotoxicity via its high oxidation potential by generating high amount of ROS. Meanwhile, alginates are known by their chelating activity and ability to bind heavy metals and toxins, in addition to their antioxidant, anti-inflammatory, and anti-apoptotic activities. So, this study aimed to explore the neuroprotective potential of sodium alginate (SA) against cellular injury, DNA damage, macromolecule alterations, and apoptosis induced by oral ingestion of Cr. Forty Wistar male rats were divided into 4 groups; group I: standard control ingested with the vehicle solution, group II: Cr-intoxicated group received 10 mg/kg b.w. of potassium dichromate orally by gavage and kept without treatment, group III: SA group in which rats were orally exposed to 200 mg/kg b.w. of SA only, and group IV: SA-treated group that received 200 mg/kg b.w. of SA along with Cr for 28 consecutive days. Neurotransmitters such as Acetyl choline esterase (AchE), Monoamine oxidase A (MAOA) concentrations, Dopamine (DA) and 5-Hydroxytryptamine (5-HT) levels were assessed in brain homogenate tissues. Neurobiochemical markers; NAD+ and S100B protein were investigated in the brain tissues and serum, respectively. Levels of HSP70, caspase-3, protein profiling were evaluated. DNA damage was determined using the Comet assay. Results revealed a significant reduction in the AchE and MAOA concentrations, DA, 5-HT, and NAD+ levels, with an increase in the S100B protein levels. Cr(VI) altered protein pattern and caused DNA damage. High levels of HSP70 and caspase-3 proteins were observed. Fortunately, oral administration of SA prevented the accumulation of Cr in brain homogenates and significantly improved all investigated parameters. SA attenuated the ROS production and relieved the oxidative stress by its active constituents. SA can protect against cellular and DNA damage and limit apoptosis. SA could be a promising neuroprotective agent against Cr(VI)-inducing toxicity.

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The success of plant breeding operations relies heavily on the nature and extent of genetic components of variation. Thus it is imperative to have reliable estimates of such components in order to formulate an efficient breeding strategy. In the present study, ten diverse lines in F2 generation were crossed to three testers viz., Giza 86(L1) ,Austuralian(L2) and their F1 Giza86 X Austuralian (L3). The parents (lines and testers) and crosses were evaluated in randomized complete block design. Analysis of variance revealed significant differences among progenies. The deviations (cultivars L1 + cultivars L2cultivars 2 L3) were analyzed to provide a test of epistasis. Additive-dominance model was fitted to the data for these traits not influenced by gene interaction. The results indicated that total epistasis was insignificant for all traits. The partitioning of the total epistasis, showed significance of ( i ) types fixable part of epistasis for all traits except lint percentage, fiber strength and micronaire, while the unfixable epistasis, dominance x dominance and dominance x additive was significant for all traits except lint percentage, fiber strength and micronaire. Additive gene action played the important role for all studied traits except for lint cotton yield, upper half mean, fiber strength and micronaire. While, dominance effects were insignificant for all traits. The degree of dominance revealed that the ratio was less than unit indicated the predominant role of additively in controlling boll weight ,seed and lint cotton yield ,seed index and uniformity ratio, whilst this ratio was equal to unity for lint percentage and upper half mean showed the important of both additive and dominance properties of genes, The higher degree of dominance for fiber strength and micronaire showed over-dominance. The results showed that the dominant alleles were dispersed between testers, as hybrids did not show any proof of directional dominance for all characters.