Exogenous GABA supplementation to facilitate Cr (III) tolerance and lipid biosynthesis in Chlorella sorokiniana.

Microalgae possess the prospective to be efficiently involved in bioremediation and biodiesel generation. However, conditions of stress often restrict their growth and diminish different metabolic processes. The current study evaluates the potential of GABA to improve the growth of the microalga Chlorella sorokiniana under Cr (III) stress through the exogenous administration of GABA. The research also investigates the concurrent impact of GABA and Cr (III) stress on various metabolic and biochemical pathways of the microalgae. In addition to the control, cultures treated with Cr (III), GABA, and both Cr (III) and GABA treated were assessed for accurately analysing the influence of GABA. The outcomes illustrated that GABA significantly promoted growth of the microalgae, resulting in higher biomass productivity (19.14 mg/L/day), lipid productivity (3.445 mg/L/day) and lipid content (18%) when compared with the cultures under Cr (III) treatment only. GABA also enhanced Chl a content (5.992 µg/ml) and percentage of protein (23.75%). FAMEs analysis by GC-MS and total lipid profile revealed that GABA treatment can boost the production of SFA and lower the level of PUFA, a distribution ideal for improving biodiesel quality. ICP-MS analysis revealed that GABA supplementation could extend Cr (III) mitigation level up to 97.7%, suggesting a potential strategy for bioremediation. This novel study demonstrates the merits of incorporating GABA in C. sorokiniana cultures under Cr (III) stress, in terms of its potential in bioremediation and biodiesel production without disrupting the pathways of photosynthesis and protein production.

Antioxidant attenuation of atrazine induced histopathological changes in testicular tissue of goat in vitro.

During the present investigation the effect of α-tocopherol (100 µmolL(-1)) in prevention of testicular toxicity induced by atrazine in goat Capra hircus have been analyzed. Vitamin E (α-tocopherol) at dose level 100 µmolL(-1) provides attenuation over the histopathological changes generated by pesticide atrazine (100 nmolml(-1)). Small pieces (approximately 1mm(3)) of testicular tissue were divided into three groups (one control group + two experimental groups). Experimental group (A) was supplemented with 100 nmolml(-1) concentration of atrazine and experimental group (B) was supplemented with 100 nmolml(-1) atrazine and 100 µmolL(-1) concentrations of vitamin E (α-Tocopherol) and harvesting was carried out after 1, 4 and 8 hrs of exposure. Control was run along with all the experimental groups. In the experimental group (A) treated with atrazine at dose level 100 nmolml(-1), revealed histomorphological alterations in the seminiferous tubule. After one hour of exposure duration small vacuoles in cytoplasm of the Sertoli cells and spermatogonia were observed. Chromolysis at pycnosis were also noticed in the spermatogonia and spermatids. In the experimental group (B) exposed with atrazine and simultaneously supplemented with Vitamin E also showed degeneration but it was milder as compared with experimental group treated with atrazine without antioxidant. Atrazine exposure induced a decline in diameter of spermatocytes from 10.51 ± 0.2052 µm in control to 7.915 ± 0.2972, 7.5 ± 0.211 and 7.14 ± 0.225 µm after exposure of 1, 4 and 8 hrs respectively but in case of atrazine supplemented with vitamin E [experimental group (B)], there was less decline in cell diameter that was 8.5 ± 0.1865, 8.1 ± 0.1201 and 7.8 ± 0.2066µm after exposure of 1, 4 and 8 hrs respectively. The result demonstrated that vitamin E delays the degenerative changes induced by atrazine.