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Drought is the major yield-limiting abiotic factor of tea cultivation. In the present study, influence of drought stress on cellular ultrastructure and antioxidants was studied drought-tolerant (TV-23) and -sensitive (S.3/A3) tea cultivars by imposing drought stress for 21 days. Drought stress led to considerable structural alterations in mitochondria, chloroplast and vacuole. Lesser membrane integrity and higher structural damage was observed in S.3/A3. Chlorophyll a, chl-b and carotenoids content in leaves decreased in each cultivar; however, the decrement was more brisk in S.3/A3. Proline, total soluble sugar, ascorbic acid and abscisic acid were elevated in TV-23 whereas hydrogen peroxide, superoxide anion, lipid peroxidation and electrolyte leakage increased rapidly in S.3/A3. Starch content decreased both in leaves and roots of each cultivar and was more pronounced in roots of TV-23. Under drought, enhanced activities of ascorbate peroxidase, catalase, peroxidase and superoxide dismutase were recorded in both roots and leaves of each cultivar, but the rate of enhancement was more in TV-23. This indicated that tolerant cultivar exhibited higher antioxidant capacity and a stronger protective mechanism such that their ultrastructural integrity was better maintained during exposure to drought stress.

In recent years we and others have shown that ascorbic acid (AH2) is a potential scavenger of superoxide (O2.-) and peroxyl (LOO.) radicals, the species involved in lipid peroxidation (LPO) in animal tissues. In this paper we have demonstrated that AH2 protects guinea pig tissues from LPO both in vivo and in vitro. The extent of LPO has been determined by estimating malonaldehyde using the thiobarbituric acid test and HPLC and also by measuring the accumulation of fluorescent pigment and occurrence of protein changes in the microsomal membranes. In AH2-deficiency, LPO occurs progressively in guinea pig tissues, despite the presence of adequate levels of antioxidants like alpha-tocopherol, GSH, protein thiols, and scavenging enzymes, namely, superoxide dismutase, catalase, and glutathione peroxidase. In a model in vitro system, microsomal LPO initiated by O2.- is completely prevented by AH2 but not by alpha-tocopherol, GSH, uric acid, and catalase. AH2 is also the most effective antioxidant in preventing microsomal LPO mediated by tert-butylhydroperoxide or the chain propagating species LOO., generated from 2,2'-azobis (2-amidinopropane) hydrochloride. The results obtained with guinea pigs may be applicable to humans, because humans are also dependent on dietary AH2. Our data suggest that an adequate vitamin C nutrition may prevent common cellular degenerative diseases associated with LPO.

One of the current theories of cardiovascular disease is that it may begin with oxygen radical-induced damages. Extensive studies have been made in different laboratories to elucidate the mechanism of oxidative damages in the presence of added iron salts. However, those in vitro studies are unlikely to be relevant to the in vivo situation, where in the normal physiological condition most of the iron remains bound with proteins. In the present study we have demonstrated that an in vitro system containing desferrioxamine, a strong iron chelator, superoxide generated by the action of xanthine oxidase on acetaldehyde initiates lipid peroxidation and protein changes in the guinea pig cardiac microsomes. We have further demonstrated that superoxide-initiated lipid peroxidation and protein changes are completely prevented by ascorbic acid. SOD also prevents but catalase, alpha-tocopherol, glutathione, uric acid, thiourea, mannitol and histidine are without effect. When NADPH is used instead of generated superoxide, the lipid peroxidation and protein changes are exclusively inhibited by ascorbic acid. SOD, catalase and other antioxidants are ineffective. The results obtained with guinea pigs may be extrapolated to humans, because like guinea pigs humans are also incapable of synthesizing ascorbic acid.

Boron (B) deficiency is prevalent in the soils of tea growing regions of India. In order to investigate the physico-chemical alterations associated with B deficiency in tea (( Camellia sinensis (L.) O. Kuntze, cv. T-78) plants, young plantlets were treated with boric acid (HBO) at 0, 2.5, and 5 μM for 8 weeks. B-scarcity decreased the photosynthetic rate ( P), stomatal conductance ( g), and transpiration ( E) alongside chlorophyll a (Chl a), chlorophyll b (Chl b), and carotenoids (Car). Superoxide anion (O), malondialdehyde (MDA), hydrogen peroxide (HO) generation and electrolyte leakage were elevated in B-deprived plants. The activities of ascorbate peroxidase (APX; EC 1.11.1.11), catalase (CAT; EC 1.11.1.6), peroxidase (POD; EC 1.11.1.7), and superoxide dismutase (SOD; EC 1.15.1.1) were increased in B-deficient plants. Simultaneously, transcripts of the antioxidant enzymes were up-regulated under B deficiency. By and large, the results suggest that B deficiency intensifies ROS generation but the antioxidant system does not provide for an adequate protection from oxidative damage. [ABSTRACT FROM AUTHOR]