Subsequently, when the cumulative doses of UVR eventually mounted up and the GST among adults decreased, the apoptotic Casp-3 was again called upon, as seen by its increase in activity. A Mepiroxol similar pattern was observed among juveniles, but since there was no detec lag in GST response, there was little need for removal of damaged cells in the initial stages of exposure. However, ChE activity decreases in this short time period suggesting that there is threshold of damage that organisms cannot prevent. Even so, as UVR doses accumulated, the same pattern of decrease in GST and increase in Casp-3 was observed. Here, we show that copepods have an enzymatic way to rapidly deal with short-term boosts in UVR exposure. D-Pantothenic acid sodium responses at molecular levels represent early warning signals and may provide useful information on how organisms respond to environmental stressors. Moreover, that several enzymes are involved suggests that neither of them is sufficient, but the combination of different enzyme systems would be necessary to reduce the stress experienced by the organism. Further experiments with mutant strains are needed to elucidate the interplay among these systems. In conclusion, our study on short-term responses mimics natural conditions experienced by zooplankton during a day with fluctuating UVR threat. Because pigments and other photoprotective compounds require lag phases of days to weeks, copepods employ the adaptation of inducing their cellular enzyme systems that have much shorter lag phases. Hence, from an evolutionary perspective, the access to several different protective systems�� behavioural, morphological, as well as rapidly mobilized enzyme systems��may considerably improve protection from stresses such as UVR and thereby increase the animal��s fitness. Oral squamous cell carcinoma is the most common head and neck cancer, with a worldwide incidence of 640,000 new cases annually. Disappointingly, survival rates of OSCC have not improved since the last many decades. Both smoked and smokeless forms of tobacco are major inducers of OSCC. Cigarette smoke has been shown to upregulate cytochrome P450 under in vitro conditions as well as in smokers. The CYP1B1 gene is transcriptionally activated by polycyclic aromatic hydrocarbons which are major constituents of cigarette smoke and tobacco, making it responsive to smoked and smokeless tobacco. CYP1B1 plays a role in the bioactivation of chemically diverse tobacco related procarcinogens to reactive metabolites. Thus, the expression of CYP1B1 is considered to be an important determinant of carcinogenesis. It has been observed that CYP1B1 is overexpressed in a wide array of human tumors compared to their respective normal tissues. Allelic variations in CYP1B1 have also been shown to modulate the incidence of several types of cancers. CYP1B1 has also been implicated in aiding resistance to tamoxifen, docetaxel and flutamide.